PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 11451040-0 2001 Interaction mechanism between indoxyl sulfate, a typical uremic toxin bound to site II, and ligands bound to site I of human serum albumin. Indican 30-45 albumin Homo sapiens 125-138 11451040-1 2001 PURPOSE: The study was performed for clarifying the mechanism of interaction between indoxyl sulfate (IS), a typical uremic toxin bound to site II, and site I-ligands when bound to human serum albumin (HSA). Indican 85-100 albumin Homo sapiens 187-200 11451040-1 2001 PURPOSE: The study was performed for clarifying the mechanism of interaction between indoxyl sulfate (IS), a typical uremic toxin bound to site II, and site I-ligands when bound to human serum albumin (HSA). Indican 102-104 albumin Homo sapiens 187-200 10926676-4 2000 Indican was transported by hSGLT1 with higher affinity (K(0.5) 0.06 mm) and 2-naphthylglucose with lower affinity (K(0.5) 0. Indican 0-7 solute carrier family 5 member 1 Homo sapiens 27-33 10681668-7 1999 The administration of indoxyl sulfate to uremic rats stimulated the expression of transforming growth factor (TGF)-beta1, tissue inhibitor of metalloproteinase (TIMP)-1 and pro-alpha1(I)collagen in the kidneys. Indican 22-37 transforming growth factor, beta 1 Rattus norvegicus 82-120 10681668-7 1999 The administration of indoxyl sulfate to uremic rats stimulated the expression of transforming growth factor (TGF)-beta1, tissue inhibitor of metalloproteinase (TIMP)-1 and pro-alpha1(I)collagen in the kidneys. Indican 22-37 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 122-168 9407462-0 1997 Indoxyl sulfate stimulates renal synthesis of transforming growth factor-beta 1 and progression of renal failure. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 46-79 9407462-1 1997 We recently demonstrated that the administration of indoxyl sulfate (dietary protein metabolite) to 5/6-nephrectomized rats accelerated the progression of chronic renal failure by increasing the transforming growth factor (TGF)-beta 1 synthesis in the kidneys, which enhanced the renal expressions of tissue inhibitor of metalloproteinase (TIMP)-1 and type 1 collagen, leading to renal fibrosis. Indican 52-67 transforming growth factor, beta 1 Rattus norvegicus 195-234 9407462-2 1997 The aim of the present study was to clarify the mechanism by which the administration of indoxyl sulfate increases TGF-beta 1 in the kidneys of uremic rats. Indican 89-104 transforming growth factor, beta 1 Rattus norvegicus 115-125 9407462-3 1997 Since infiltrative monocytes are suggested to be an important source of TGF-beta 1 in tubulointerstitial fibrosis, we examined the effect of indoxyl sulfate administration to uremic rats on the renal gene expression of intercellular adhesion molecule (ICAM)-1, which is involved in the infiltration of monocytes to kidneys. Indican 141-156 intercellular adhesion molecule 1 Rattus norvegicus 219-259 9407462-4 1997 Indoxyl sulfate administration was observed to enhance the mRNA levels of ICAM-1 as well as those of TGF-beta 1, TIMP-1 and pro alpha 1 (I) collagen in the renal cortex of 5/6-nephrectomized uremic rats. Indican 0-15 intercellular adhesion molecule 1 Rattus norvegicus 74-80 9407462-4 1997 Indoxyl sulfate administration was observed to enhance the mRNA levels of ICAM-1 as well as those of TGF-beta 1, TIMP-1 and pro alpha 1 (I) collagen in the renal cortex of 5/6-nephrectomized uremic rats. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 101-111 9407455-7 1997 We conclude that AST-120 administration concurrent with LPD may be superior to LPD alone in retarding the progression of CRF by inhibiting accumulation of indoxyl sulfate. Indican 155-170 acyl-CoA synthetase bubblegum family member 1 Homo sapiens 56-59 9407462-4 1997 Indoxyl sulfate administration was observed to enhance the mRNA levels of ICAM-1 as well as those of TGF-beta 1, TIMP-1 and pro alpha 1 (I) collagen in the renal cortex of 5/6-nephrectomized uremic rats. Indican 0-15 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 113-119 9407462-5 1997 In addition, we demonstrated in vitro that the addition of indoxyl sulfate significantly increased the synthesis of TGF-beta 1 in cultured proximal tubular cells. Indican 59-74 transforming growth factor, beta 1 Rattus norvegicus 116-126 9407462-6 1997 Thus, the overload of indoxyl sulfate in uremic kidneys increased the infiltration of monocytes and directly increased the synthesis of TGF-beta 1 in proximal tubular cells. Indican 22-37 transforming growth factor, beta 1 Rattus norvegicus 136-146 9350672-0 1997 Indoxyl sulfate increases the gene expressions of TGF-beta 1, TIMP-1 and pro-alpha 1(I) collagen in uremic rat kidneys. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 50-60 9350672-0 1997 Indoxyl sulfate increases the gene expressions of TGF-beta 1, TIMP-1 and pro-alpha 1(I) collagen in uremic rat kidneys. Indican 0-15 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 62-68 9350672-5 1997 In the first experiment, the administration of indoxyl sulfate for five weeks significantly increased the mRNA levels of TGF-beta 1, TIMP-1 and pro-alpha 1(I) collagen in the uremic rats given indoxyl sulfate compared with the control uremic rats, accompanied by a significant decline in renal function and worsening of glomerular sclerosis. Indican 47-62 transforming growth factor, beta 1 Rattus norvegicus 121-131 9350672-5 1997 In the first experiment, the administration of indoxyl sulfate for five weeks significantly increased the mRNA levels of TGF-beta 1, TIMP-1 and pro-alpha 1(I) collagen in the uremic rats given indoxyl sulfate compared with the control uremic rats, accompanied by a significant decline in renal function and worsening of glomerular sclerosis. Indican 47-62 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 133-139 9350672-5 1997 In the first experiment, the administration of indoxyl sulfate for five weeks significantly increased the mRNA levels of TGF-beta 1, TIMP-1 and pro-alpha 1(I) collagen in the uremic rats given indoxyl sulfate compared with the control uremic rats, accompanied by a significant decline in renal function and worsening of glomerular sclerosis. Indican 193-208 transforming growth factor, beta 1 Rattus norvegicus 121-131 9350672-5 1997 In the first experiment, the administration of indoxyl sulfate for five weeks significantly increased the mRNA levels of TGF-beta 1, TIMP-1 and pro-alpha 1(I) collagen in the uremic rats given indoxyl sulfate compared with the control uremic rats, accompanied by a significant decline in renal function and worsening of glomerular sclerosis. Indican 193-208 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 133-139 9350672-7 1997 In conclusion, these findings indicate that the overload of the protein metabolite indoxyl sulfate on remnant nephrons is involved in the increased bioactivity of TGF-beta 1 in uremic kidneys, which enhances the renal expression of TIMP-1 and type 1 collagen, leading to the progression of CRF. Indican 83-98 transforming growth factor, beta 1 Rattus norvegicus 163-173 9350672-7 1997 In conclusion, these findings indicate that the overload of the protein metabolite indoxyl sulfate on remnant nephrons is involved in the increased bioactivity of TGF-beta 1 in uremic kidneys, which enhances the renal expression of TIMP-1 and type 1 collagen, leading to the progression of CRF. Indican 83-98 TIMP metallopeptidase inhibitor 1 Rattus norvegicus 232-238 9350673-2 1997 In the present study, we determined whether an oral adsorbent (AST-120) could reduce the serum and urine levels of indoxyl sulfate and suppress the progression of chronic renal failure (CRF) in undialyzed uremic patients. Indican 115-130 solute carrier family 17 member 5 Homo sapiens 63-66 9350673-5 1997 Administration of AST-120 significantly decreased the serum and urine levels of indoxyl sulfate, and tended to improve the slope of the 1/SCr-time plot in the CRF patients. Indican 80-95 solute carrier family 17 member 5 Homo sapiens 18-21 9350673-6 1997 Among the patients in whom urinary excretion of indoxyl sulfate was reduced by AST-120, the oral adsorbent significantly improved the slope of the 1/SCr-time plot. Indican 48-63 solute carrier family 17 member 5 Homo sapiens 79-82 8861801-1 1996 The content of indoxyl-beta-D-glucuronide, which has been found in patients" plasma as a new indicator of renal failure, logarithmically correlated with that of 3-indoxyl sulfate (indican) in the plasma of hemodialysis patients, showing another weak correlation with beta(2)-microglobulin content. Indican 161-178 beta-2-microglobulin Homo sapiens 267-288 9387112-2 1997 In this study we determined if a low-protein diet or oral sorbent (AST-120) could reduce the serum and urine levels of indoxyl sulfate in 5/6-nephrectomized uremic rats and undialyzed uremic patients. Indican 119-134 solute carrier family 17 member 5 Homo sapiens 67-70 9387112-4 1997 The serum and urine levels of indoxyl sulfate dramatically decreased 1-2 days after fasting or AST-120 treatment. Indican 30-45 solute carrier family 17 member 5 Homo sapiens 95-98 9387112-7 1997 Administration of AST-120 significantly decreased serum and urine levels of indoxyl sulfate in 22 undialyzed uremic patients. Indican 76-91 solute carrier family 17 member 5 Homo sapiens 18-21 9387112-8 1997 In conclusion, a low-protein diet or AST-120 reduced the serum and urine levels of indoxyl sulfate, a stimulating factor for glomerular sclerosis, in both uremic rats and undialyzed uremic patients. Indican 83-98 solute carrier family 17 member 5 Homo sapiens 37-40 8861801-1 1996 The content of indoxyl-beta-D-glucuronide, which has been found in patients" plasma as a new indicator of renal failure, logarithmically correlated with that of 3-indoxyl sulfate (indican) in the plasma of hemodialysis patients, showing another weak correlation with beta(2)-microglobulin content. Indican 180-187 beta-2-microglobulin Homo sapiens 267-288 2120492-5 1990 Since indoxyl sulfate is bound to serum albumin, it cannot be removed efficiently by hemodialysis, and it tends to accumulate in uremic serum. Indican 6-21 albumin Rattus norvegicus 34-47 33232689-0 2021 Indoxyl sulfate induces ROS production via the aryl hydrocarbon receptor-NADPH oxidase pathway and inactivates NO in vascular tissues. Indican 0-15 aryl hydrocarbon receptor Rattus norvegicus 47-72 34941711-0 2021 Indoxyl Sulfate Elevated Lnc-SLC15A1-1 Upregulating CXCL10/CXCL8 Expression in High-Glucose Endothelial Cells by Sponging MicroRNAs. Indican 0-15 solute carrier family 15 member 1 Homo sapiens 29-36 34941746-0 2021 Indoxyl Sulfate Contributes to mTORC1-Induced Renal Fibrosis via The OAT/NADPH Oxidase/ROS Pathway. Indican 0-15 CREB regulated transcription coactivator 1 Mus musculus 31-37 34941746-4 2021 Among the seven protein-bound uremic toxins, only indoxyl sulfate (IS) caused significant activation of mTORC1 in human kidney 2 cells (HK-2 cells). Indican 50-65 CREB regulated transcription coactivator 1 Mus musculus 104-110 26925780-1 2016 OBJECTIVE: The uremic toxin Indoxyl-3-sulphate (IS), a ligand of Aryl hydrocarbon Receptor (AhR), raises in blood during early renal dysfunction as a consequence of tubular damage, which may be present even when eGFR is normal or only moderately reduced, and promotes cardiovascular damage and monocyte-macrophage activation. Indican 28-46 aryl hydrocarbon receptor Homo sapiens 65-90 26925780-1 2016 OBJECTIVE: The uremic toxin Indoxyl-3-sulphate (IS), a ligand of Aryl hydrocarbon Receptor (AhR), raises in blood during early renal dysfunction as a consequence of tubular damage, which may be present even when eGFR is normal or only moderately reduced, and promotes cardiovascular damage and monocyte-macrophage activation. Indican 28-46 aryl hydrocarbon receptor Homo sapiens 92-95 26925780-1 2016 OBJECTIVE: The uremic toxin Indoxyl-3-sulphate (IS), a ligand of Aryl hydrocarbon Receptor (AhR), raises in blood during early renal dysfunction as a consequence of tubular damage, which may be present even when eGFR is normal or only moderately reduced, and promotes cardiovascular damage and monocyte-macrophage activation. Indican 28-46 epidermal growth factor receptor Homo sapiens 212-216 34941711-0 2021 Indoxyl Sulfate Elevated Lnc-SLC15A1-1 Upregulating CXCL10/CXCL8 Expression in High-Glucose Endothelial Cells by Sponging MicroRNAs. Indican 0-15 C-X-C motif chemokine ligand 10 Homo sapiens 52-58 34941711-0 2021 Indoxyl Sulfate Elevated Lnc-SLC15A1-1 Upregulating CXCL10/CXCL8 Expression in High-Glucose Endothelial Cells by Sponging MicroRNAs. Indican 0-15 C-X-C motif chemokine ligand 8 Homo sapiens 59-64 34941677-7 2021 As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1. Indican 184-199 GLI family zinc finger 2 Homo sapiens 114-119 34600152-0 2021 The effect of dihydroceramide desaturase 1 inhibition on endothelial impairment induced by indoxyl sulfate. Indican 91-106 delta 4-desaturase, sphingolipid 1 Homo sapiens 14-42 34600152-3 2021 This study assessed the therapeutic potential of dihydroceramide desaturase 1 (Des1) inhibition, the last enzyme involved in de novo ceramide synthesis, to mitigate the vascular effects of the PBUT indoxyl sulfate (IS). Indican 215-217 delta 4-desaturase, sphingolipid 1 Homo sapiens 79-83 34941677-7 2021 As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1. Indican 184-199 caspase 4 Homo sapiens 267-276 34941677-7 2021 As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1. Indican 184-199 caspase 5 Homo sapiens 277-286 34941677-7 2021 As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1. Indican 184-199 caspase 8 Homo sapiens 310-319 34941677-7 2021 As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1. Indican 184-199 caspase 1 Homo sapiens 324-333 35316209-3 2022 Here we report the findings that memory CD4-T cells and plasma samples of INR from several cohorts are enriched in gut-derived bacterial solutes (GDBS) p-cresol-sulfate (PCS) and indoxyl sulfate (IS) that both negatively correlated with CD4-T cell counts. Indican 179-194 CD4 molecule Homo sapiens 40-43 34638892-0 2021 Syndecan-1 and Free Indoxyl Sulfate Levels Are Associated with miR-126 in Chronic Kidney Disease. Indican 20-35 microRNA 126 Homo sapiens 63-70 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 81-96 NLR family pyrin domain containing 3 Homo sapiens 173-178 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 81-96 caspase 1 Homo sapiens 180-189 34678967-0 2021 The Influence of OAT1 Density and Functionality on Indoxyl Sulfate Transport in the Human Proximal Tubule: An Integrated Computational and In Vitro Study. Indican 51-66 solute carrier family 22 member 6 Homo sapiens 17-21 34678967-6 2021 In this integrated experimental-computational study, we developed a PT computational model that focuses on indoxyl sulfate (IS) transport by organic anionic transporter 1 (OAT1), capturing the transporter density in detail along the basolateral cell membrane as well as the activity of the transporter and the inward boundary flux. Indican 107-122 solute carrier family 22 member 6 Homo sapiens 141-170 34678967-6 2021 In this integrated experimental-computational study, we developed a PT computational model that focuses on indoxyl sulfate (IS) transport by organic anionic transporter 1 (OAT1), capturing the transporter density in detail along the basolateral cell membrane as well as the activity of the transporter and the inward boundary flux. Indican 107-122 solute carrier family 22 member 6 Homo sapiens 172-176 34678967-6 2021 In this integrated experimental-computational study, we developed a PT computational model that focuses on indoxyl sulfate (IS) transport by organic anionic transporter 1 (OAT1), capturing the transporter density in detail along the basolateral cell membrane as well as the activity of the transporter and the inward boundary flux. Indican 124-126 solute carrier family 22 member 6 Homo sapiens 141-170 34678967-6 2021 In this integrated experimental-computational study, we developed a PT computational model that focuses on indoxyl sulfate (IS) transport by organic anionic transporter 1 (OAT1), capturing the transporter density in detail along the basolateral cell membrane as well as the activity of the transporter and the inward boundary flux. Indican 124-126 solute carrier family 22 member 6 Homo sapiens 172-176 34357946-5 2021 In vitro studies showed that fraxetin and indoxyl sulfate had no cytotoxic effects on MES13 kidney cells, but that fraxetin significantly decreased IS-induced cell motility and decreased protein expression of alpha-SMA, N-cadherin, vimentin, and Collagen IV via the ERK-mediated signaling pathway. Indican 42-57 actin alpha 2, smooth muscle, aorta Mus musculus 209-218 34357946-5 2021 In vitro studies showed that fraxetin and indoxyl sulfate had no cytotoxic effects on MES13 kidney cells, but that fraxetin significantly decreased IS-induced cell motility and decreased protein expression of alpha-SMA, N-cadherin, vimentin, and Collagen IV via the ERK-mediated signaling pathway. Indican 42-57 cadherin 2 Mus musculus 220-230 34357946-5 2021 In vitro studies showed that fraxetin and indoxyl sulfate had no cytotoxic effects on MES13 kidney cells, but that fraxetin significantly decreased IS-induced cell motility and decreased protein expression of alpha-SMA, N-cadherin, vimentin, and Collagen IV via the ERK-mediated signaling pathway. Indican 42-57 vimentin Mus musculus 232-240 34357946-5 2021 In vitro studies showed that fraxetin and indoxyl sulfate had no cytotoxic effects on MES13 kidney cells, but that fraxetin significantly decreased IS-induced cell motility and decreased protein expression of alpha-SMA, N-cadherin, vimentin, and Collagen IV via the ERK-mediated signaling pathway. Indican 42-57 mitogen-activated protein kinase 1 Mus musculus 266-269 34716244-2 2021 Urem ic solutes such as indoxyl sulfate (IS) and kynurenine (Kyn) mediate prothrombotic effect through tissue factor (TF). Indican 24-39 coagulation factor III Mus musculus 103-116 34716244-2 2021 Urem ic solutes such as indoxyl sulfate (IS) and kynurenine (Kyn) mediate prothrombotic effect through tissue factor (TF). Indican 24-39 coagulation factor III Mus musculus 118-120 34716244-2 2021 Urem ic solutes such as indoxyl sulfate (IS) and kynurenine (Kyn) mediate prothrombotic effect through tissue factor (TF). Indican 41-43 coagulation factor III Mus musculus 103-116 34716244-2 2021 Urem ic solutes such as indoxyl sulfate (IS) and kynurenine (Kyn) mediate prothrombotic effect through tissue factor (TF). Indican 41-43 coagulation factor III Mus musculus 118-120 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 81-96 interleukin 1 alpha Homo sapiens 194-202 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 81-96 interleukin 1 alpha Homo sapiens 245-253 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 81-96 caspase 1 Homo sapiens 268-277 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 98-100 NLR family pyrin domain containing 3 Homo sapiens 173-178 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 98-100 caspase 1 Homo sapiens 180-189 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 98-100 interleukin 1 alpha Homo sapiens 194-202 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 98-100 interleukin 1 alpha Homo sapiens 245-253 34680443-4 2021 Exposure of human conditionally immortalized proximal tubule epithelial cells to indoxyl sulfate (IS) and a mixture of anionic PBUTs (UT mix) increased expression levels of NLRP3, caspase-1 and IL-1beta, accompanied by a significant increase in IL-1beta secretion and caspase-1 activity. Indican 98-100 caspase 1 Homo sapiens 268-277 34137923-0 2021 Correction to: Indoxyl sulfate enhances endothelin-1-induced contraction via impairment of NO/cGMP signaling in rat aorta. Indican 15-30 endothelin 1 Rattus norvegicus 40-52 34110802-9 2021 A function verification study proved that chlormethiazole, a widely used CYP2E1 inhibitor, could reduce the production of indoxyl sulfate in the liver and attenuate cisplatin-induced AKI in rats. Indican 122-137 cytochrome P450, family 2, subfamily e, polypeptide 1 Rattus norvegicus 73-79 35112184-8 2022 The XPR1 mRNA expression in cultured VCMCs was also unaffected by administration of indoxyl sulfate or calcitriol deficiency but was decreased by 1-34 parathyroid hormone or fibroblast growth factor 23 supplementation. Indican 84-99 xenotropic and polytropic retrovirus receptor 1 Mus musculus 4-8 34021781-0 2021 Indoxyl sulfate enhances endothelin-1-induced contraction via impairment of NO/cGMP signaling in rat aorta. Indican 0-15 endothelin 1 Rattus norvegicus 25-37 35088197-0 2022 Indoxyl Sulfate Activates NLRP3 Inflammasome to Induce Cardiac Contractile Dysfunction Accompanied by Myocardial Fibrosis and Hypertrophy. Indican 0-15 NLR family, pyrin domain containing 3 Rattus norvegicus 26-31 35392531-11 2022 CONCLUSIONS: Our results indicated that UA improves the IS-induced impairment of mitochondrial biogenesis by affecting differentiation, ATP levels, and IL-6 secretion in C2C12 cells. Indican 56-58 interleukin 6 Mus musculus 152-156 35138387-6 2022 RESULTS: At 20-weeks post-5/6Nx, L34-treated mice showed significantly lesser renal injuries, as evaluated by i) kidney fibrosis area (P < 0.01) with lower serum creatinine and proteinuria, ii) GDUT including trimethylamine-N-oxide (TMAO) (P = 0.02) and indoxyl sulfate (P < 0.01), and iii) endotoxin (P = 0.03) and serum TNF-alpha (P = 0.01), than 5/6Nx-controls. Indican 254-269 lectin, galactose binding, soluble 3 Mus musculus 33-36 35138387-8 2022 After incubation with indoxyl sulfate, Caco-2 enterocytes had higher IL-8, NFkappaB expression, and lower TEER value, and HK2 cells demonstrated higher gene expression of TNF-alpha, IL-6, and collagen (type III and type IV). Indican 22-37 chemokine (C-X-C motif) ligand 15 Mus musculus 69-73 35138387-8 2022 After incubation with indoxyl sulfate, Caco-2 enterocytes had higher IL-8, NFkappaB expression, and lower TEER value, and HK2 cells demonstrated higher gene expression of TNF-alpha, IL-6, and collagen (type III and type IV). Indican 22-37 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 75-83 35138387-8 2022 After incubation with indoxyl sulfate, Caco-2 enterocytes had higher IL-8, NFkappaB expression, and lower TEER value, and HK2 cells demonstrated higher gene expression of TNF-alpha, IL-6, and collagen (type III and type IV). Indican 22-37 tumor necrosis factor Mus musculus 171-180 35138387-8 2022 After incubation with indoxyl sulfate, Caco-2 enterocytes had higher IL-8, NFkappaB expression, and lower TEER value, and HK2 cells demonstrated higher gene expression of TNF-alpha, IL-6, and collagen (type III and type IV). Indican 22-37 interleukin 6 Mus musculus 182-186 35138387-9 2022 These indoxyl sulfate-activated parameters were attenuated with L34-conditioned media indicating the protective role of L34 on enterocyte integrity and renal fibrogenesis. Indican 6-21 lectin, galactose binding, soluble 3 Mus musculus 120-123 35276782-7 2022 LPS and indoxyl sulfate demonstrated co-toxicity to endothelial cells inducing reactive oxygen species, E-selectin, and monocyte chemoattractant protein-1 (MCP-1) production. Indican 8-23 selectin E Homo sapiens 104-114 35276782-7 2022 LPS and indoxyl sulfate demonstrated co-toxicity to endothelial cells inducing reactive oxygen species, E-selectin, and monocyte chemoattractant protein-1 (MCP-1) production. Indican 8-23 C-C motif chemokine ligand 2 Homo sapiens 120-154 35276782-7 2022 LPS and indoxyl sulfate demonstrated co-toxicity to endothelial cells inducing reactive oxygen species, E-selectin, and monocyte chemoattractant protein-1 (MCP-1) production. Indican 8-23 C-C motif chemokine ligand 2 Homo sapiens 156-161 34752422-3 2022 Here, we show that the dietary tryptophan-derived uremic solute including indoxyl sulfate (IS) and Kynurenine (Kyn), at concentrations corresponding to CKD patients suppressed beta-catenin in several cell-types including microvascular endothelial cells (EC), inhibiting Wnt activity and proangiogenic Wnt targets in ECs. Indican 74-89 catenin beta 1 Homo sapiens 176-188 34752422-3 2022 Here, we show that the dietary tryptophan-derived uremic solute including indoxyl sulfate (IS) and Kynurenine (Kyn), at concentrations corresponding to CKD patients suppressed beta-catenin in several cell-types including microvascular endothelial cells (EC), inhibiting Wnt activity and proangiogenic Wnt targets in ECs. Indican 91-93 catenin beta 1 Homo sapiens 176-188 34021781-11 2021 A cell-permeant superoxide scavenger reduced the ET-1-induced contraction in the indoxyl sulfate group. Indican 81-96 endothelin 1 Rattus norvegicus 49-53 34021781-13 2021 The present study revealed that indoxyl sulfate augments ET-1-induced contraction in rat aortae. Indican 32-47 endothelin 1 Rattus norvegicus 57-61 35246616-0 2022 Indoxyl sulfate- and P-cresol-induced monocyte adhesion and migration is mediated by integrin-linked kinase-dependent podosome formation. Indican 0-15 integrin linked kinase Homo sapiens 85-107 35204244-10 2022 Blockade of AhR reversed low Sp1 activity caused by IS. Indican 52-54 aryl hydrocarbon receptor Homo sapiens 12-15 35164316-4 2022 The study further synthesized the human serum albumin (HSA)-PNIPAAm conjugate, taking the advantage that HSA can specifically adsorb indoxyl sulfate (IS) as a uremic toxin. Indican 133-148 albumin Homo sapiens 40-53 35164316-4 2022 The study further synthesized the human serum albumin (HSA)-PNIPAAm conjugate, taking the advantage that HSA can specifically adsorb indoxyl sulfate (IS) as a uremic toxin. Indican 150-152 albumin Homo sapiens 40-53 35063244-1 2022 BACKGROUND & AIMS: Patients with Chronic Kidney Disease (CKD) have an imbalance in the gut microbiota that can lead to increase levels of lipopolysaccharides (LPS) and uremic toxins such as indoxyl sulfate (IS), p-cresyl sulfate (p-CS), and indole-3 acetic acid (IAA). Indican 190-205 citrate synthase Homo sapiens 232-234 35063244-1 2022 BACKGROUND & AIMS: Patients with Chronic Kidney Disease (CKD) have an imbalance in the gut microbiota that can lead to increase levels of lipopolysaccharides (LPS) and uremic toxins such as indoxyl sulfate (IS), p-cresyl sulfate (p-CS), and indole-3 acetic acid (IAA). Indican 207-209 citrate synthase Homo sapiens 232-234 34021781-2 2021 Here, we examined the effects of indoxyl sulfate on endothelin-1 (ET-1)-induced contraction in rat thoracic aortas. Indican 33-48 endothelin 1 Rattus norvegicus 52-64 34021781-2 2021 Here, we examined the effects of indoxyl sulfate on endothelin-1 (ET-1)-induced contraction in rat thoracic aortas. Indican 33-48 endothelin 1 Rattus norvegicus 66-70 34021781-3 2021 Indoxyl sulfate (10-3 M, 60 min) increased ET-1-induced contraction but did not affect isotonic high-K+-induced contraction. Indican 0-15 endothelin 1 Rattus norvegicus 43-47 34021781-4 2021 The ET-1-induced contraction was enhanced by endothelial denudation in both control and indoxyl sulfate-treated groups. Indican 88-103 endothelin 1 Rattus norvegicus 4-8 34021781-5 2021 BQ123 (10-6 M), an ETA receptor antagonist, reduced the ET-1-induced contraction in both control and indoxyl sulfate groups. Indican 101-116 endothelin 1 Rattus norvegicus 56-60 34021781-8 2021 L-NNA, an NO synthase (NOS) inhibitor, increased the ET-1-induced contractions in both the control and indoxyl sulfate groups, whereas L-NPA (10-6 M), a specific neuronal NOS inhibitor, did not affect the ET-1-induced contraction in both groups. Indican 103-118 endothelin 1 Rattus norvegicus 53-57 33790363-0 2021 Hypouricemic agents reduce indoxyl sulfate excretion by inhibiting the renal transporters OAT1/3 and ABCG2. Indican 27-42 solute carrier family 22 member 6 Rattus norvegicus 90-96 33631173-0 2021 Apoptosis signal-regulating kinase 1 inhibition reverses deleterious indoxyl sulfate-mediated endothelial effects. Indican 69-84 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 0-36 33631173-3 2021 This study assessed the therapeutic potential of ASK1 inhibition in alleviating endothelial effects induced by IS. Indican 111-113 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 49-53 33631173-9 2021 SIGNIFICANCE: ASK1 inhibition attenuated vasorelaxation and endothelial cell migration impaired by IS. Indican 99-101 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 14-18 33911115-9 2021 In C2C12 myotubes stimulated with IS, although beta2-AR activation also attenuated myotube size reduction and ROS accumulation as did other anti-oxidant reagents, it failed to augment the mitochondrial membrane potential. Indican 34-36 adenosine A2a receptor Mus musculus 47-55 33387144-0 2021 Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation by regulation of beta-catenin and YAP pathways. Indican 13-28 catenin beta 1 Homo sapiens 93-105 33387144-0 2021 Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation by regulation of beta-catenin and YAP pathways. Indican 13-28 Yes1 associated transcriptional regulator Homo sapiens 110-113 33387144-13 2021 In addition, this study provided evidences that activation of beta-catenin or inhibition of YAP could alleviate IS-induced inflammatory response in LPS-stimulated macrophages. Indican 112-114 catenin beta 1 Homo sapiens 62-74 33387144-13 2021 In addition, this study provided evidences that activation of beta-catenin or inhibition of YAP could alleviate IS-induced inflammatory response in LPS-stimulated macrophages. Indican 112-114 Yes1 associated transcriptional regulator Homo sapiens 92-95 33790363-0 2021 Hypouricemic agents reduce indoxyl sulfate excretion by inhibiting the renal transporters OAT1/3 and ABCG2. Indican 27-42 ATP binding cassette subfamily G member 2 Rattus norvegicus 101-106 33578912-0 2021 Suppressed Hepatic Production of Indoxyl Sulfate Attenuates Cisplatin-Induced Acute Kidney Injury in Sulfotransferase 1a1-Deficient Mice. Indican 33-48 sulfotransferase family 1A, phenol-preferring, member 1 Mus musculus 101-121 33658826-13 2021 Plasma levels of blood urea nitrogen, creatinine, indoxyl sulfate, IL-1beta and renal tubular injury were increased in mice after renal I/R and were decreased by AST-120 treatment. Indican 50-65 solute carrier family 17 member 5 Homo sapiens 162-165 33578912-2 2021 Here, we demonstrate the toxico-pathological roles of indoxyl sulfate (IS), a sulfate-conjugated uremic toxin, and sulfotransferase 1A1 (SULT1A1), an enzyme involved in its synthesis, in cisplatin-induced acute kidney injury using Sult1a1-deficient (Sult1a1-/- KO) mice. Indican 54-69 sulfotransferase family 1A, phenol-preferring, member 1 Mus musculus 231-238 33578912-2 2021 Here, we demonstrate the toxico-pathological roles of indoxyl sulfate (IS), a sulfate-conjugated uremic toxin, and sulfotransferase 1A1 (SULT1A1), an enzyme involved in its synthesis, in cisplatin-induced acute kidney injury using Sult1a1-deficient (Sult1a1-/- KO) mice. Indican 54-69 sulfotransferase family 1A, phenol-preferring, member 1 Mus musculus 250-257 33437209-7 2021 Furthermore, p-cresol and indoxyl sulfate gradually increased senescence-associated beta-galactosidase positive cells while upregulated the expression of p21 which participate in senescent process. Indican 26-41 galactosidase beta 1 Homo sapiens 84-102 33484425-11 2021 CONCLUSIONS: The present meta-analysis demonstrated that prebiotics, synbiotics, and AST-120 can effectively reduce both serum indoxyl sulfate and p-cresyl sulfate in CKD patients when compared with placebo. Indican 127-142 solute carrier family 17 member 5 Homo sapiens 85-88 33458837-0 2021 The role of AMP-activated protein kinase alpha1-mediated endoplasmic reticulum stress in alleviating the toxic effect of uremic toxin indoxyl sulfate on vascular endothelial cells by Klotho. Indican 134-149 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 12-40 33458837-0 2021 The role of AMP-activated protein kinase alpha1-mediated endoplasmic reticulum stress in alleviating the toxic effect of uremic toxin indoxyl sulfate on vascular endothelial cells by Klotho. Indican 134-149 BCL2 related protein A1 Homo sapiens 41-47 33458837-0 2021 The role of AMP-activated protein kinase alpha1-mediated endoplasmic reticulum stress in alleviating the toxic effect of uremic toxin indoxyl sulfate on vascular endothelial cells by Klotho. Indican 134-149 klotho Homo sapiens 183-189 33458837-5 2021 Treatment with Klotho significantly attenuated IS-induced above effects. Indican 47-49 klotho Homo sapiens 15-21 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 klotho Homo sapiens 13-19 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 75-117 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-109 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 klotho Homo sapiens 260-266 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 intercellular adhesion molecule 1 Homo sapiens 282-315 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 intercellular adhesion molecule 1 Homo sapiens 317-323 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 vascular cell adhesion molecule 1 Homo sapiens 329-362 33458837-6 2021 Furthermore, Klotho alleviated the IS toxic effect on HUVECs via promoting AMP-activated protein kinase (AMPK) alpha1 phosphorylation instead of directly upregulating AMPKalpha1, which could be partly blocked by AMPK pathway inhibitor-Compound C. In addition, Klotho also inhibited intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression induced by IS. Indican 35-37 vascular cell adhesion molecule 1 Homo sapiens 364-370 33458837-7 2021 Altogether, these results indicated that Klotho can protect HUVECs from IS-induced injury by alleviating AMPKalpha1-mediated endoplasmic reticulum stress. Indican 72-74 klotho Homo sapiens 41-47 33458837-7 2021 Altogether, these results indicated that Klotho can protect HUVECs from IS-induced injury by alleviating AMPKalpha1-mediated endoplasmic reticulum stress. Indican 72-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 105-115 33430226-0 2021 Indoxyl Sulfate Mediates the Low Inducibility of the NLRP3 Inflammasome in Hemodialysis Patients. Indican 0-15 NLR family pyrin domain containing 3 Homo sapiens 53-58 33406025-0 2021 Indoxyl sulfate impairs angiogenesis via chronic aryl hydrocarbon receptor activation. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 49-74 33406025-4 2021 In this study, activation of the aryl hydrocarbon receptor (AHR) via indoxyl sulfate, a known uremic metabolite, was found to impair endothelial cell tube formation and proliferation but not migratory function. Indican 69-84 aryl hydrocarbon receptor Homo sapiens 33-58 33406025-4 2021 In this study, activation of the aryl hydrocarbon receptor (AHR) via indoxyl sulfate, a known uremic metabolite, was found to impair endothelial cell tube formation and proliferation but not migratory function. Indican 69-84 aryl hydrocarbon receptor Homo sapiens 60-63 33406025-5 2021 Moreover, aortic ring cultures treated with indoxyl sulfate also exhibited decreased sprouting and high AHR activation. Indican 44-59 aryl hydrocarbon receptor Homo sapiens 104-107 33215785-8 2021 BDNF was also correlated with body weight, hemodialysis vintage, and serum levels of total protein and indoxyl sulfate but not with body mass index, appendicular skeletal muscle mass, serum interleukin 6 levels, or J-PHQ-9 scores. Indican 103-118 brain derived neurotrophic factor Homo sapiens 0-4 32757783-5 2021 METHODS: Indoxyl sulfate (IS), p-cresol (PC), and uremic sera from CKD patients were used to stimulate PAR-2 expression in normal human epidermal keratinocytes (NHEKs). Indican 9-24 F2R like trypsin receptor 1 Homo sapiens 103-108 32757783-5 2021 METHODS: Indoxyl sulfate (IS), p-cresol (PC), and uremic sera from CKD patients were used to stimulate PAR-2 expression in normal human epidermal keratinocytes (NHEKs). Indican 26-28 F2R like trypsin receptor 1 Homo sapiens 103-108 32757783-9 2021 Soybean trypsin inhibitor significantly decreased PAR-2 mRNA and protein expression in NHEKs treated with IS, PC, and CKD sera. Indican 106-108 F2R like trypsin receptor 1 Homo sapiens 50-55 33437209-7 2021 Furthermore, p-cresol and indoxyl sulfate gradually increased senescence-associated beta-galactosidase positive cells while upregulated the expression of p21 which participate in senescent process. Indican 26-41 H3 histone pseudogene 16 Homo sapiens 154-157 33120292-12 2021 Dojuksan significantly increased basal FNDC5 expression and inhibited TNFalpha-induced and indoxyl sulfate-induced FNDC5 down-regulation in C2C12 cells. Indican 91-106 fibronectin type III domain containing 5 Mus musculus 115-120 33066667-3 2020 AhR, when binding with exogenous ligands (environmental pollutants such as polycylic aryl hydrocarbon (PAH), dioxins) or endogenous ligand indoxyl-sulfate (IS), has dual functions that are mediated by the nature of the binding ligand, binding time, and specific pathways of distinct ligands. Indican 139-154 aryl hydrocarbon receptor Homo sapiens 0-3 32979364-12 2020 We demonstrate that IS promotes the HASMCs phenotype switch by suppressing MGP expression via ROS/NF-kappaB/miR-155-5p signaling and provide a new insight for the pathogenesis of IS-induced VC. Indican 20-22 matrix Gla protein Rattus norvegicus 75-78 32979364-12 2020 We demonstrate that IS promotes the HASMCs phenotype switch by suppressing MGP expression via ROS/NF-kappaB/miR-155-5p signaling and provide a new insight for the pathogenesis of IS-induced VC. Indican 20-22 nuclear factor kappa B subunit 1 Homo sapiens 98-107 32979364-12 2020 We demonstrate that IS promotes the HASMCs phenotype switch by suppressing MGP expression via ROS/NF-kappaB/miR-155-5p signaling and provide a new insight for the pathogenesis of IS-induced VC. Indican 20-22 microRNA 155 Homo sapiens 108-115 33227547-0 2020 CREB/ATF3 signaling mediates indoxyl sulfate-induced vascular smooth muscle cell proliferation and neointimal formation in uremia. Indican 29-44 cAMP responsive element binding protein 1 Homo sapiens 0-4 33227547-0 2020 CREB/ATF3 signaling mediates indoxyl sulfate-induced vascular smooth muscle cell proliferation and neointimal formation in uremia. Indican 29-44 activating transcription factor 3 Homo sapiens 5-9 33227547-5 2020 METHODS AND RESULTS: Treatment of VSMCs with uremic toxin (indoxyl sulfate [IS]) activated cAMP/CREB/ATF3/cyclin D signaling, which was reflected by increased VSMC proliferation. Indican 59-74 cAMP responsive element binding protein 1 Homo sapiens 96-100 33227547-5 2020 METHODS AND RESULTS: Treatment of VSMCs with uremic toxin (indoxyl sulfate [IS]) activated cAMP/CREB/ATF3/cyclin D signaling, which was reflected by increased VSMC proliferation. Indican 59-74 activating transcription factor 3 Homo sapiens 101-105 32055962-10 2020 Urinary excretion of 3-indoxyl sulfate, a metabolized form of gut bacteria-derived indole, was significantly higher in Ido1-/- than in Ido1+/+ mice. Indican 21-38 indoleamine 2,3-dioxygenase 1 Mus musculus 119-123 32055962-10 2020 Urinary excretion of 3-indoxyl sulfate, a metabolized form of gut bacteria-derived indole, was significantly higher in Ido1-/- than in Ido1+/+ mice. Indican 21-38 indoleamine 2,3-dioxygenase 1 Mus musculus 135-139 32979364-0 2020 Indoxyl sulfate promotes osteogenic differentiation of vascular smooth muscle cells by miR-155-5p-dependent downregulation of matrix Gla protein via ROS/NF-kappaB signaling. Indican 0-15 microRNA 155 Homo sapiens 87-94 32979364-0 2020 Indoxyl sulfate promotes osteogenic differentiation of vascular smooth muscle cells by miR-155-5p-dependent downregulation of matrix Gla protein via ROS/NF-kappaB signaling. Indican 0-15 matrix Gla protein Homo sapiens 126-144 32979364-0 2020 Indoxyl sulfate promotes osteogenic differentiation of vascular smooth muscle cells by miR-155-5p-dependent downregulation of matrix Gla protein via ROS/NF-kappaB signaling. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 153-162 33066667-3 2020 AhR, when binding with exogenous ligands (environmental pollutants such as polycylic aryl hydrocarbon (PAH), dioxins) or endogenous ligand indoxyl-sulfate (IS), has dual functions that are mediated by the nature of the binding ligand, binding time, and specific pathways of distinct ligands. Indican 156-158 aryl hydrocarbon receptor Homo sapiens 0-3 33050543-0 2020 Indoxylsulfate, a Metabolite of the Microbiome, Has Cytostatic Effects in Breast Cancer via Activation of AHR and PXR Receptors and Induction of Oxidative Stress. Indican 0-14 nuclear receptor subfamily 1 group I member 2 Homo sapiens 114-117 33050543-0 2020 Indoxylsulfate, a Metabolite of the Microbiome, Has Cytostatic Effects in Breast Cancer via Activation of AHR and PXR Receptors and Induction of Oxidative Stress. Indican 0-14 aryl hydrocarbon receptor Homo sapiens 106-109 33050571-0 2020 Resveratrol Rescue Indoxyl Sulfate-Induced Deterioration of Osteoblastogenesis via the Aryl Hydrocarbon Receptor /MAPK Pathway. Indican 19-34 aryl hydrocarbon receptor Homo sapiens 87-112 33050571-1 2020 Indoxyl sulfate (IS), a uremic toxin derived from dietary tryptophan metabolism by the gut microbiota, is an endogenous aryl hydrocarbon receptor (AhR) agonist and a key player in bone remodeling. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 120-145 33050571-1 2020 Indoxyl sulfate (IS), a uremic toxin derived from dietary tryptophan metabolism by the gut microbiota, is an endogenous aryl hydrocarbon receptor (AhR) agonist and a key player in bone remodeling. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 147-150 33050571-1 2020 Indoxyl sulfate (IS), a uremic toxin derived from dietary tryptophan metabolism by the gut microbiota, is an endogenous aryl hydrocarbon receptor (AhR) agonist and a key player in bone remodeling. Indican 17-19 aryl hydrocarbon receptor Homo sapiens 120-145 33050571-1 2020 Indoxyl sulfate (IS), a uremic toxin derived from dietary tryptophan metabolism by the gut microbiota, is an endogenous aryl hydrocarbon receptor (AhR) agonist and a key player in bone remodeling. Indican 17-19 aryl hydrocarbon receptor Homo sapiens 147-150 33162798-0 2020 Indoxyl Sulfate-induced Vascular Calcification is mediated through Altered Notch Signaling Pathway in Vascular Smooth Muscle Cells. Indican 0-15 notch receptor 1 Rattus norvegicus 75-80 33162798-1 2020 Introduction: The aim of this study was to determine the role of Notch in indoxyl sulfate (IS)-induced vascular calcification (VC). Indican 74-89 notch receptor 1 Rattus norvegicus 65-70 33162798-1 2020 Introduction: The aim of this study was to determine the role of Notch in indoxyl sulfate (IS)-induced vascular calcification (VC). Indican 91-93 notch receptor 1 Rattus norvegicus 65-70 32468073-5 2020 It further demonstrated that indoxyl sulfate inhibited the expression of Klotho protein. Indican 29-44 klotho Mus musculus 73-79 32867359-0 2020 TRPV1 Hyperfunction Involved in Uremic Toxin Indoxyl Sulfate-Mediated Renal Tubular Damage. Indican 45-60 transient receptor potential cation channel subfamily V member 1 Canis lupus familiaris 0-5 32867359-10 2020 Blockade of ALOX12 by cinnamyl-3,4-dihydroxy-alpha-cyanocinnamate or baicalein attenuated the effects of IS. Indican 105-107 arachidonate 12-lipoxygenase, 12S type Canis lupus familiaris 12-18 32867359-11 2020 Since aryl hydrocarbon receptor (AhR) activation after IS binding is crucial in mediating cell death, here, we found that the AhR blockade not only ameliorated tubular damage but also attenuated ALOX12 expression and 12(S)-HETE production caused by IS. Indican 55-57 aryl hydrocarbon receptor Canis lupus familiaris 6-31 32867359-11 2020 Since aryl hydrocarbon receptor (AhR) activation after IS binding is crucial in mediating cell death, here, we found that the AhR blockade not only ameliorated tubular damage but also attenuated ALOX12 expression and 12(S)-HETE production caused by IS. Indican 55-57 aryl hydrocarbon receptor Canis lupus familiaris 33-36 32867359-11 2020 Since aryl hydrocarbon receptor (AhR) activation after IS binding is crucial in mediating cell death, here, we found that the AhR blockade not only ameliorated tubular damage but also attenuated ALOX12 expression and 12(S)-HETE production caused by IS. Indican 55-57 aryl hydrocarbon receptor Canis lupus familiaris 126-129 32867359-14 2020 Further study on TRPV1 may attenuate kidney susceptibility to the functional loss of end-stage kidney disease via IS. Indican 114-116 transient receptor potential cation channel subfamily V member 1 Canis lupus familiaris 17-22 32593718-0 2020 Indoxyl sulfate promotes the atherosclerosis through up-regulating the miR-34a expression in endothelial cells and vascular smooth muscle cells in vitro. Indican 0-15 microRNA 34a Homo sapiens 71-78 32544852-5 2020 The HPD induced increases in serum levels of l-carnitine, indoxyl sulfate, and phenylacetylglutamine but not TMAO or p-cresyl sulfate. Indican 58-73 4-hydroxyphenylpyruvate dioxygenase Homo sapiens 4-7 32593718-7 2020 However, inhibition of the miR-34a abolished these effects of IS in vitro, indicating that miR-34a is involved in the development of AS induced by IS. Indican 62-64 microRNA 34a Homo sapiens 27-34 32593718-7 2020 However, inhibition of the miR-34a abolished these effects of IS in vitro, indicating that miR-34a is involved in the development of AS induced by IS. Indican 62-64 microRNA 34a Homo sapiens 91-98 32593718-7 2020 However, inhibition of the miR-34a abolished these effects of IS in vitro, indicating that miR-34a is involved in the development of AS induced by IS. Indican 147-149 microRNA 34a Homo sapiens 27-34 32593718-7 2020 However, inhibition of the miR-34a abolished these effects of IS in vitro, indicating that miR-34a is involved in the development of AS induced by IS. Indican 147-149 microRNA 34a Homo sapiens 91-98 32593718-11 2020 Consistently, blockage of miR-34a abolished the remarkable effects on protein expressions induced by IS. Indican 101-103 microRNA 34a Homo sapiens 26-33 32439179-5 2020 The uremic toxin, indoxyl sulfate, activated the autophagy flux through modulation of FTO and m6A modifications in RNA. Indican 18-33 FTO alpha-ketoglutarate dependent dioxygenase Homo sapiens 86-89 32439179-6 2020 Notably, knockdown of FTO or inhibit the m6A by 3-deazaadenosine blocks the effects of indoxyl sulfate on autophagy activation in cells. Indican 87-102 FTO alpha-ketoglutarate dependent dioxygenase Homo sapiens 22-25 32527975-2 2020 Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AhR), which is widely expressed in the central nervous system and which we previously identified as the receptor of indoxyl sulfate in endothelial cells. Indican 25-40 aryl hydrocarbon receptor Rattus norvegicus 83-108 32527975-2 2020 Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AhR), which is widely expressed in the central nervous system and which we previously identified as the receptor of indoxyl sulfate in endothelial cells. Indican 25-40 aryl hydrocarbon receptor Homo sapiens 110-113 32527975-2 2020 Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AhR), which is widely expressed in the central nervous system and which we previously identified as the receptor of indoxyl sulfate in endothelial cells. Indican 226-241 aryl hydrocarbon receptor Rattus norvegicus 83-108 32527975-2 2020 Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AhR), which is widely expressed in the central nervous system and which we previously identified as the receptor of indoxyl sulfate in endothelial cells. Indican 226-241 aryl hydrocarbon receptor Homo sapiens 110-113 32527975-8 2020 In addition, non-CKD AhR-/- knockout mice were protected against indoxyl sulfate-induced blood-brain barrier disruption and cognitive impairment. Indican 65-80 aryl-hydrocarbon receptor Mus musculus 21-24 32527975-9 2020 CONCLUSIONS: AhR activation by indoxyl sulfate, a uremic toxin, leads to blood-brain barrier disruption associated with cognitive impairment in animal models of CKD. Indican 31-46 aryl-hydrocarbon receptor Mus musculus 13-16 32641998-0 2020 Indoxyl sulfate induces intestinal barrier injury through IRF1-DRP1 axis-mediated mitophagy impairment. Indican 0-15 interferon regulatory factor 1 Mus musculus 58-62 32641998-0 2020 Indoxyl sulfate induces intestinal barrier injury through IRF1-DRP1 axis-mediated mitophagy impairment. Indican 0-15 dynamin 1-like Mus musculus 63-67 32544852-6 2020 Urinary excretion of l-carnitine, indoxyl sulfate, phenylacetylglutamine, and TMA increased with the HPD but not TMAO or p-cresyl sulfate. Indican 34-49 4-hydroxyphenylpyruvate dioxygenase Homo sapiens 101-104 32260098-1 2020 Cardiovascular complications observed in chronic kidney disease (CKD) are associated with aryl hydrocarbon receptor (AhR) activation by tryptophan-derived uremic toxins-mainly indoxyl sulfate (IS). Indican 176-191 aryl-hydrocarbon receptor Mus musculus 90-115 32429048-0 2020 Concentration and Duration of Indoxyl Sulfate Exposure Affects Osteoclastogenesis by Regulating NFATc1 via Aryl Hydrocarbon Receptor. Indican 30-45 nuclear factor of activated T cells 1 Homo sapiens 96-102 32429048-0 2020 Concentration and Duration of Indoxyl Sulfate Exposure Affects Osteoclastogenesis by Regulating NFATc1 via Aryl Hydrocarbon Receptor. Indican 30-45 aryl hydrocarbon receptor Homo sapiens 107-132 32429048-1 2020 Indoxyl sulfate (IS) is a chronic kidney disease (CKD)-specific renal osteodystrophy metabolite that affects the nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), a transcription factor promoting osteoclastogenesis. Indican 0-15 nuclear factor of activated T cells 1 Homo sapiens 113-163 32429048-1 2020 Indoxyl sulfate (IS) is a chronic kidney disease (CKD)-specific renal osteodystrophy metabolite that affects the nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), a transcription factor promoting osteoclastogenesis. Indican 0-15 nuclear factor of activated T cells 1 Homo sapiens 165-171 32429048-1 2020 Indoxyl sulfate (IS) is a chronic kidney disease (CKD)-specific renal osteodystrophy metabolite that affects the nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), a transcription factor promoting osteoclastogenesis. Indican 17-19 nuclear factor of activated T cells 1 Homo sapiens 113-163 32429048-1 2020 Indoxyl sulfate (IS) is a chronic kidney disease (CKD)-specific renal osteodystrophy metabolite that affects the nuclear factor of activated T-cells, cytoplasmic 1 (NFATc1), a transcription factor promoting osteoclastogenesis. Indican 17-19 nuclear factor of activated T cells 1 Homo sapiens 165-171 32464602-0 2020 Klotho alleviates indoxyl sulfate-induced heart failure and kidney damage by promoting M2 macrophage polarization. Indican 18-33 klotho Homo sapiens 0-6 32464602-8 2020 A reduction in IS-induced phosphorylation of NF-kB p65 was observed in response to Klotho overexpression, suggesting that Klotho alleviates kidney and cardiac injury by inactivating NF-kB signaling and promoting macrophage M2 polarization. Indican 15-17 RELA proto-oncogene, NF-kB subunit Homo sapiens 51-54 32464602-8 2020 A reduction in IS-induced phosphorylation of NF-kB p65 was observed in response to Klotho overexpression, suggesting that Klotho alleviates kidney and cardiac injury by inactivating NF-kB signaling and promoting macrophage M2 polarization. Indican 15-17 klotho Homo sapiens 83-89 32464602-8 2020 A reduction in IS-induced phosphorylation of NF-kB p65 was observed in response to Klotho overexpression, suggesting that Klotho alleviates kidney and cardiac injury by inactivating NF-kB signaling and promoting macrophage M2 polarization. Indican 15-17 klotho Homo sapiens 122-128 32435647-13 2020 DNA damage was induced by IS stimulation as confirmed by elevated protein level of p-ATM, p-ATR, p-BRCA1, and p-p53 in T cells. Indican 26-28 ATM serine/threonine kinase Homo sapiens 85-88 32435647-13 2020 DNA damage was induced by IS stimulation as confirmed by elevated protein level of p-ATM, p-ATR, p-BRCA1, and p-p53 in T cells. Indican 26-28 ATR serine/threonine kinase Homo sapiens 92-95 32435647-13 2020 DNA damage was induced by IS stimulation as confirmed by elevated protein level of p-ATM, p-ATR, p-BRCA1, and p-p53 in T cells. Indican 26-28 BRCA1 DNA repair associated Homo sapiens 99-104 32435647-13 2020 DNA damage was induced by IS stimulation as confirmed by elevated protein level of p-ATM, p-ATR, p-BRCA1, and p-p53 in T cells. Indican 26-28 tumor protein p53 Homo sapiens 112-115 31448977-9 2020 Furthermore, cell line study showed that ciprofloxacin inhibited the OAT3-mediated transport of IS. Indican 96-98 solute carrier family 22 member 8 Rattus norvegicus 69-73 32260098-1 2020 Cardiovascular complications observed in chronic kidney disease (CKD) are associated with aryl hydrocarbon receptor (AhR) activation by tryptophan-derived uremic toxins-mainly indoxyl sulfate (IS). Indican 176-191 aryl-hydrocarbon receptor Mus musculus 117-120 32260098-1 2020 Cardiovascular complications observed in chronic kidney disease (CKD) are associated with aryl hydrocarbon receptor (AhR) activation by tryptophan-derived uremic toxins-mainly indoxyl sulfate (IS). Indican 193-195 aryl-hydrocarbon receptor Mus musculus 90-115 32260098-1 2020 Cardiovascular complications observed in chronic kidney disease (CKD) are associated with aryl hydrocarbon receptor (AhR) activation by tryptophan-derived uremic toxins-mainly indoxyl sulfate (IS). Indican 193-195 aryl-hydrocarbon receptor Mus musculus 117-120 32244284-0 2020 Aryl Hydrocarbon Receptor Activation and Tissue Factor Induction by Fluid Shear Stress and Indoxyl Sulfate in Endothelial Cells. Indican 91-106 aryl hydrocarbon receptor Homo sapiens 0-25 32124946-0 2020 Lactobacillus salivarius BP121 prevents cisplatin-induced acute kidney injury by inhibition of uremic toxins such as indoxyl sulfate and p-cresol sulfate via alleviating dysbiosis. Indican 117-132 Blood pressure QTL 121 Rattus norvegicus 25-30 32124946-5 2020 BP121 prevented cisplatin-induced AKI in rats, as demonstrated by decreases in inflammation and oxidative stress in kidney tissue and in serum levels of uremic toxins such as indoxyl sulfate (IS) and p-cresol sulfate (PCS). Indican 175-190 Blood pressure QTL 121 Rattus norvegicus 0-5 32244284-0 2020 Aryl Hydrocarbon Receptor Activation and Tissue Factor Induction by Fluid Shear Stress and Indoxyl Sulfate in Endothelial Cells. Indican 91-106 coagulation factor III, tissue factor Homo sapiens 41-54 32244284-1 2020 Endogenous agonists of the transcription factor aryl hydrocarbon receptor (AHR) such as the indolic uremic toxin, indoxyl sulfate (IS), accumulate in patients with chronic kidney disease. Indican 114-129 aryl hydrocarbon receptor Homo sapiens 48-73 32244284-1 2020 Endogenous agonists of the transcription factor aryl hydrocarbon receptor (AHR) such as the indolic uremic toxin, indoxyl sulfate (IS), accumulate in patients with chronic kidney disease. Indican 114-129 aryl hydrocarbon receptor Homo sapiens 75-78 32244284-1 2020 Endogenous agonists of the transcription factor aryl hydrocarbon receptor (AHR) such as the indolic uremic toxin, indoxyl sulfate (IS), accumulate in patients with chronic kidney disease. Indican 131-133 aryl hydrocarbon receptor Homo sapiens 48-73 32244284-1 2020 Endogenous agonists of the transcription factor aryl hydrocarbon receptor (AHR) such as the indolic uremic toxin, indoxyl sulfate (IS), accumulate in patients with chronic kidney disease. Indican 131-133 aryl hydrocarbon receptor Homo sapiens 75-78 32045570-0 2020 Uremic toxin indoxyl sulfate suppresses myocardial Cx43 assembly and expression via JNK activation. Indican 13-28 gap junction protein, alpha 1 Rattus norvegicus 51-55 32045570-0 2020 Uremic toxin indoxyl sulfate suppresses myocardial Cx43 assembly and expression via JNK activation. Indican 13-28 mitogen-activated protein kinase 8 Rattus norvegicus 84-87 31932072-7 2020 The pattern of beta-galactosidase increase coincided with the changes in serum indoxyl sulfate levels. Indican 79-94 galactosidase, beta 1 Mus musculus 15-33 31721030-6 2020 Treatment of preadipocytes with another known endogenous AhR agonist, indoxyl sulfate (IS), followed by differentiation also blocked the NE-stimulated upregulation of UCP1. Indican 70-85 aryl hydrocarbon receptor Homo sapiens 57-60 31721030-6 2020 Treatment of preadipocytes with another known endogenous AhR agonist, indoxyl sulfate (IS), followed by differentiation also blocked the NE-stimulated upregulation of UCP1. Indican 70-85 uncoupling protein 1 Homo sapiens 167-171 31721030-6 2020 Treatment of preadipocytes with another known endogenous AhR agonist, indoxyl sulfate (IS), followed by differentiation also blocked the NE-stimulated upregulation of UCP1. Indican 87-89 aryl hydrocarbon receptor Homo sapiens 57-60 31721030-6 2020 Treatment of preadipocytes with another known endogenous AhR agonist, indoxyl sulfate (IS), followed by differentiation also blocked the NE-stimulated upregulation of UCP1. Indican 87-89 uncoupling protein 1 Homo sapiens 167-171 31721030-7 2020 Knockdown of the aryl hydrocarbon receptor (AhR) caused the preadipocytes to be refractory to PCB126 and IS effects. Indican 105-107 aryl hydrocarbon receptor Homo sapiens 17-42 31721030-7 2020 Knockdown of the aryl hydrocarbon receptor (AhR) caused the preadipocytes to be refractory to PCB126 and IS effects. Indican 105-107 aryl hydrocarbon receptor Homo sapiens 44-47 31721030-10 2020 These results indicate that exposure of preadipocytes to endogenous (IS) or exogenous (PCB126) AhR agonists is effective at blocking them from becoming functional adipocytes that are capable of the beiging response. Indican 69-71 aryl hydrocarbon receptor Homo sapiens 95-98 31932072-8 2020 Machine-learning-based image quantification revealed positive correlations between indoxyl sulfate levels and beta-galactosidase expression in various tissues. Indican 83-98 galactosidase, beta 1 Mus musculus 110-128 31932072-9 2020 This pattern of beta-galactosidase expression was recapitulated in the indoxyl sulfate-specific model. Indican 71-86 galactosidase, beta 1 Mus musculus 16-34 31932072-10 2020 The ischemia/reperfusion injury model showed increase in beta-galactosidase in renal tubules that persisted despite reduction in serum indoxyl sulfate and blood urea nitrogen levels. Indican 135-150 galactosidase, beta 1 Mus musculus 57-75 31932072-11 2020 Thus, our results demonstrate a relationship between AHR activation in various tissues of mice with CKD or AKI and the levels of indoxyl sulfate. Indican 129-144 aryl-hydrocarbon receptor Mus musculus 53-56 31820187-0 2020 MicroRNA-214 targets COX-2 to antagonize indoxyl sulfate (IS)-induced endothelial cell apoptosis. Indican 41-56 microRNA 214 Homo sapiens 0-12 31837804-3 2020 Here, we demonstrate that uremic toxins indoxyl sulfate (IxS), p-cresyl sulfate (pCS) and indole acetic acid (IAA) are incorporated by human endothelial cells and inhibit the autophagic flux, demonstrated by cellular p62 accumulation. Indican 40-55 nucleoporin 62 Homo sapiens 217-220 31837804-3 2020 Here, we demonstrate that uremic toxins indoxyl sulfate (IxS), p-cresyl sulfate (pCS) and indole acetic acid (IAA) are incorporated by human endothelial cells and inhibit the autophagic flux, demonstrated by cellular p62 accumulation. Indican 57-60 nucleoporin 62 Homo sapiens 217-220 31820187-0 2020 MicroRNA-214 targets COX-2 to antagonize indoxyl sulfate (IS)-induced endothelial cell apoptosis. Indican 41-56 mitochondrially encoded cytochrome c oxidase II Homo sapiens 21-26 31820187-0 2020 MicroRNA-214 targets COX-2 to antagonize indoxyl sulfate (IS)-induced endothelial cell apoptosis. Indican 58-60 microRNA 214 Homo sapiens 0-12 31820187-0 2020 MicroRNA-214 targets COX-2 to antagonize indoxyl sulfate (IS)-induced endothelial cell apoptosis. Indican 58-60 mitochondrially encoded cytochrome c oxidase II Homo sapiens 21-26 31862563-5 2020 The dialysate supported by cationic liposomes also exhibited better clearing efficiency for IS (PEI-20: 57.65 +- 1.74 %; Oct-5: 62.80 +- 0.69 %; CTAB-10: 66.54 +- 0.91 %; p < 0.05) and p-cresol (PEI-20: 67.05 +- 3.09 %; Oct-5: 79.26 +- 0.43 %; CTAB-5: 68.45 +- 1.72 %; p < 0.05) than for phosphate buffer saline (IS: 29.70 +- 2.38 %; p-cresol: 33.59 +- 3.44 %) or dialysate supported by bovine serum albumin (IS: 50.00 +- 4.01 %; p-cresol: 53.06 +- 0.97 %). Indican 92-94 albumin Homo sapiens 400-413 31697949-0 2019 METTL14-Dependent m6A Regulates Vascular Calcification Induced by Indoxyl Sulfate. Indican 66-81 methyltransferase 14, N6-adenosine-methyltransferase subunit Homo sapiens 0-7 31746392-5 2020 The present study revealed that the expression of the CYP1B1 gene was significantly (P<0.05, CKD or IS vs. control) upregulated by CKD serum or IS at the transcriptional and translational level. Indican 103-105 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 54-60 31746392-5 2020 The present study revealed that the expression of the CYP1B1 gene was significantly (P<0.05, CKD or IS vs. control) upregulated by CKD serum or IS at the transcriptional and translational level. Indican 147-149 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 54-60 31746392-6 2020 Furthermore, IS treatment resulted in the nuclear translocation of aryl hydrocarbon receptor (AhR), an endogenous ligand of IS. Indican 13-15 aryl hydrocarbon receptor Homo sapiens 67-92 31746392-6 2020 Furthermore, IS treatment resulted in the nuclear translocation of aryl hydrocarbon receptor (AhR), an endogenous ligand of IS. Indican 13-15 aryl hydrocarbon receptor Homo sapiens 94-97 31746392-6 2020 Furthermore, IS treatment resulted in the nuclear translocation of aryl hydrocarbon receptor (AhR), an endogenous ligand of IS. Indican 124-126 aryl hydrocarbon receptor Homo sapiens 67-92 31746392-6 2020 Furthermore, IS treatment resulted in the nuclear translocation of aryl hydrocarbon receptor (AhR), an endogenous ligand of IS. Indican 124-126 aryl hydrocarbon receptor Homo sapiens 94-97 31536856-0 2020 1,25(OH)2 D3 attenuates indoxyl sulfate-induced epithelial-to-mesenchymal cell transition via inactivation of PI3K/Akt/beta-catenin signaling in renal tubular epithelial cells. Indican 24-39 AKT serine/threonine kinase 1 Homo sapiens 115-118 31536856-0 2020 1,25(OH)2 D3 attenuates indoxyl sulfate-induced epithelial-to-mesenchymal cell transition via inactivation of PI3K/Akt/beta-catenin signaling in renal tubular epithelial cells. Indican 24-39 catenin beta 1 Homo sapiens 119-131 31536856-8 2020 Pretreatment with 1,25(OH)2 D3 and LY294002 (phosphoinositide 3-kinase [PIK3] inhibitor) significantly inhibited the IS-induced phosphorylation of Akt and beta-catenin, nuclear beta-catenin accumulation, and EMT-associated protein expression. Indican 117-119 phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Homo sapiens 72-76 31536856-8 2020 Pretreatment with 1,25(OH)2 D3 and LY294002 (phosphoinositide 3-kinase [PIK3] inhibitor) significantly inhibited the IS-induced phosphorylation of Akt and beta-catenin, nuclear beta-catenin accumulation, and EMT-associated protein expression. Indican 117-119 AKT serine/threonine kinase 1 Homo sapiens 147-150 31536856-8 2020 Pretreatment with 1,25(OH)2 D3 and LY294002 (phosphoinositide 3-kinase [PIK3] inhibitor) significantly inhibited the IS-induced phosphorylation of Akt and beta-catenin, nuclear beta-catenin accumulation, and EMT-associated protein expression. Indican 117-119 catenin beta 1 Homo sapiens 155-167 31536856-8 2020 Pretreatment with 1,25(OH)2 D3 and LY294002 (phosphoinositide 3-kinase [PIK3] inhibitor) significantly inhibited the IS-induced phosphorylation of Akt and beta-catenin, nuclear beta-catenin accumulation, and EMT-associated protein expression. Indican 117-119 catenin beta 1 Homo sapiens 177-189 31697949-0 2019 METTL14-Dependent m6A Regulates Vascular Calcification Induced by Indoxyl Sulfate. Indican 66-81 glycoprotein M6A Homo sapiens 18-21 31697949-4 2019 We modulated the expression of METTL14 using siRNAs (in vitro) to study its function in regulating HASMCs m6A, osteoblasts induced by indoxyl sulfate. Indican 134-149 methyltransferase 14, N6-adenosine-methyltransferase subunit Homo sapiens 31-38 31697949-6 2019 KEY FINDINGS: We discovered that the METTL14 expression increases in calcific arteries and in HASMCs induced by indoxyl sulfate, thereby increasing the m6A level in RNA and decreasing the vascular repair function. Indican 112-127 methyltransferase 14, N6-adenosine-methyltransferase subunit Homo sapiens 37-44 31697949-6 2019 KEY FINDINGS: We discovered that the METTL14 expression increases in calcific arteries and in HASMCs induced by indoxyl sulfate, thereby increasing the m6A level in RNA and decreasing the vascular repair function. Indican 112-127 glycoprotein M6A Homo sapiens 152-155 31697949-7 2019 Decreasing the expression of METTL14 in calcified arteries attenuated the indoxyl sulfate-induced increase in m6A and decrease in HASMCs calcification. Indican 74-89 methyltransferase 14, N6-adenosine-methyltransferase subunit Homo sapiens 29-36 31697949-7 2019 Decreasing the expression of METTL14 in calcified arteries attenuated the indoxyl sulfate-induced increase in m6A and decrease in HASMCs calcification. Indican 74-89 glycoprotein M6A Homo sapiens 110-113 31697949-8 2019 We performed the methylation activity of METTL14, which selectively methylates vascular osteogenic transcripts, thereby promoting their degradation and improving their protein expression induced by indoxyl sulfate. Indican 198-213 methyltransferase 14, N6-adenosine-methyltransferase subunit Homo sapiens 41-48 30849338-0 2019 Indoxyl sulfate induces myotube atrophy by ROS-ERK and JNK-MAFbx cascades. Indican 0-15 mitogen-activated protein kinase 1 Mus musculus 47-50 31885805-0 2019 Role of Resveratrol on Indoxyl Sulfate-Induced Endothelial Hyperpermeability via Aryl Hydrocarbon Receptor (AHR)/Src-Dependent Pathway. Indican 23-38 aryl hydrocarbon receptor Homo sapiens 81-106 31885805-0 2019 Role of Resveratrol on Indoxyl Sulfate-Induced Endothelial Hyperpermeability via Aryl Hydrocarbon Receptor (AHR)/Src-Dependent Pathway. Indican 23-38 aryl hydrocarbon receptor Homo sapiens 108-111 31885805-0 2019 Role of Resveratrol on Indoxyl Sulfate-Induced Endothelial Hyperpermeability via Aryl Hydrocarbon Receptor (AHR)/Src-Dependent Pathway. Indican 23-38 SRC proto-oncogene, non-receptor tyrosine kinase Homo sapiens 113-116 31885805-2 2019 Tryptophan metabolite-derived indoxyl sulfate (IS) is identified as one of the uremic toxins and physiological endogenous ligand/activator of aryl hydrocarbon receptor (AHR), associated with atherosclerosis in chronic kidney disease (CKD) patients. Indican 30-45 aryl hydrocarbon receptor Homo sapiens 142-167 31885805-2 2019 Tryptophan metabolite-derived indoxyl sulfate (IS) is identified as one of the uremic toxins and physiological endogenous ligand/activator of aryl hydrocarbon receptor (AHR), associated with atherosclerosis in chronic kidney disease (CKD) patients. Indican 30-45 aryl hydrocarbon receptor Homo sapiens 169-172 31382511-0 2019 Indoxyl Sulfate Stimulates Angiogenesis by Regulating Reactive Oxygen Species Production via CYP1B1. Indican 0-15 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 93-99 31382511-7 2019 Notably, the pro-angiogenic response of IS and increased ROS production were abolished when CYP1B1, one of the main target genes that was highly upregulated by IS, was silenced. Indican 40-42 cytochrome P450 family 1 subfamily B member 1 Homo sapiens 92-98 31153139-6 2019 Moreover, mRNA expression of Nrg4 was investigated in cultured, differentiated mouse brown and white adipocytes, as well as hepatocytes, after treatment with the uremic toxin indoxyl sulfate. Indican 175-190 neuregulin 4 Mus musculus 29-33 31448474-0 2019 Indoxyl sulfate-induced calcification of vascular smooth muscle cells via the PI3K/Akt/NF-kappaB signaling pathway. Indican 0-15 AKT serine/threonine kinase 1 Homo sapiens 83-86 31448474-0 2019 Indoxyl sulfate-induced calcification of vascular smooth muscle cells via the PI3K/Akt/NF-kappaB signaling pathway. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 87-96 31448474-9 2019 Together, these results suggest that PI3K/Akt/NK-kappaB signaling plays an important role in the pathogenesis of osteogenic transdifferentiation induced by IS. Indican 156-158 AKT serine/threonine kinase 1 Homo sapiens 42-45 31679996-7 2019 Rare pLOF variants in the genes BTN3A2, ENPEP, and GEM that have been associated with blood pressure in UK Biobank, were associated with vasoactive metabolites indoxyl sulfate, asymmetric dimethylarginine (ADMA), and with niacinamide, respectively. Indican 160-175 butyrophilin subfamily 3 member A2 Homo sapiens 32-38 31679996-7 2019 Rare pLOF variants in the genes BTN3A2, ENPEP, and GEM that have been associated with blood pressure in UK Biobank, were associated with vasoactive metabolites indoxyl sulfate, asymmetric dimethylarginine (ADMA), and with niacinamide, respectively. Indican 160-175 glutamyl aminopeptidase Homo sapiens 40-45 31411076-13 2019 The data suggest that meprin beta activity enhances diabetic kidney injury in part by altering the metabolite balance in kidneys, favoring high levels of uremic toxins such as indoxyl sulfate and N-Methyl-pyridone-carboxamide. Indican 176-191 meprin 1 beta Mus musculus 22-33 31284759-0 2019 Indoxyl sulfate-induced TNF-alpha is regulated by crosstalk between the aryl hydrocarbon receptor, NF-kappaB, and SOCS2 in human macrophages. Indican 0-15 tumor necrosis factor Homo sapiens 24-33 31284759-0 2019 Indoxyl sulfate-induced TNF-alpha is regulated by crosstalk between the aryl hydrocarbon receptor, NF-kappaB, and SOCS2 in human macrophages. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 72-97 31284759-0 2019 Indoxyl sulfate-induced TNF-alpha is regulated by crosstalk between the aryl hydrocarbon receptor, NF-kappaB, and SOCS2 in human macrophages. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 99-108 31284759-0 2019 Indoxyl sulfate-induced TNF-alpha is regulated by crosstalk between the aryl hydrocarbon receptor, NF-kappaB, and SOCS2 in human macrophages. Indican 0-15 suppressor of cytokine signaling 2 Homo sapiens 114-119 31284759-3 2019 Thus, we investigated the underlying molecular mechanisms involved in IS-induced production of TNF-alpha, a major cardiotoxic cytokine, by human macrophages. Indican 70-72 tumor necrosis factor Homo sapiens 95-104 31207307-9 2019 In vivo, along with the increase of IS and decrease of Klotho in the serum, the activation of RIG-I/NF-kappaB signaling was observed in peripheral blood monocytes in both CKD mice and patients. Indican 36-38 DEAD/H box helicase 58 Mus musculus 94-99 31207307-9 2019 In vivo, along with the increase of IS and decrease of Klotho in the serum, the activation of RIG-I/NF-kappaB signaling was observed in peripheral blood monocytes in both CKD mice and patients. Indican 36-38 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 100-109 31341083-3 2019 Remote metabolite sensing and signaling was observed in kidneys from healthy volunteers and rats in vivo, leading to induced OAT1 expression and increased removal of indoxyl sulfate, a prototypical microbiome-derived metabolite and uremic toxin. Indican 166-181 solute carrier family 22 member 6 Rattus norvegicus 125-129 31341083-4 2019 Using 2D and 3D human proximal tubule cell models, we show that indoxyl sulfate induces OAT1 via AhR and EGFR signaling, controlled by miR-223. Indican 64-79 solute carrier family 22 member 6 Homo sapiens 88-92 31341083-4 2019 Using 2D and 3D human proximal tubule cell models, we show that indoxyl sulfate induces OAT1 via AhR and EGFR signaling, controlled by miR-223. Indican 64-79 aryl hydrocarbon receptor Homo sapiens 97-100 31341083-4 2019 Using 2D and 3D human proximal tubule cell models, we show that indoxyl sulfate induces OAT1 via AhR and EGFR signaling, controlled by miR-223. Indican 64-79 epidermal growth factor receptor Homo sapiens 105-109 31341083-4 2019 Using 2D and 3D human proximal tubule cell models, we show that indoxyl sulfate induces OAT1 via AhR and EGFR signaling, controlled by miR-223. Indican 64-79 microRNA 223 Homo sapiens 135-142 30849338-0 2019 Indoxyl sulfate induces myotube atrophy by ROS-ERK and JNK-MAFbx cascades. Indican 0-15 mitogen-activated protein kinase 8 Mus musculus 55-58 30849338-0 2019 Indoxyl sulfate induces myotube atrophy by ROS-ERK and JNK-MAFbx cascades. Indican 0-15 F-box protein 32 Mus musculus 59-64 31023251-15 2019 Annotated meprin beta expression-associated metabolites with strong variable importance in projection (VIP) scores play roles in lipid metabolism (LysoPC(16:1(9Z)), taurocholic acid), amino acid metabolism (indoxyl sulfate, hippuric acid), and neurotransmitter/stress hormone synthesis (cortisol, 3-methoxy-4-hydroxyphenylethylene glycolsulfate, homovanillic acid sulfate). Indican 207-222 meprin 1 beta Mus musculus 10-21 30940651-7 2019 Additional metabolic linkage to these pathways revealed that IS and PCS exposure engendered a prodiabetic state evidenced by elevated resting glucose and reduced GLUT1 expression. Indican 61-63 solute carrier family 2 member 1 Homo sapiens 162-167 30826567-10 2019 Only plasma indoxyl sulfate concentration was significantly higher in recipients with CYP3A phenoconversion compared to those without phenoconversion. Indican 12-27 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 86-91 31178953-9 2019 Our study demonstrates that the IS increase promotes renal fibroblast activation by a HSP90-dependent pathway and indicates HSP90 inhibition as a potential strategy to restrain IS-induced kidney inflammation and fibrosis in CKD. Indican 32-34 heat shock protein, 3 Mus musculus 86-91 30826567-3 2019 Indoxyl sulfate, parathyroid hormone (PTH), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-alpha) have been reported to cause CYP3A downregulation in renal failure. Indican 0-15 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 138-143 31001934-1 2019 BACKGROUND: Removal of uremic toxins such as indoxyl sulfate by AST-120 is known to improve renal function and delay the initiation of dialysis in patients with advanced chronic kidney disease. Indican 45-60 solute carrier family 17 member 5 Homo sapiens 64-67 30912928-1 2019 Recent studies have suggested that uremic toxins such as indoxyl sulfate (IS) and indole-3-acetic acid (IAA) from the metabolism of the gut microbiota may be involved in the inflammatory signaling pathway in chronic kidney disease (CKD) patients through the activation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor. Indican 57-72 aryl hydrocarbon receptor Homo sapiens 276-301 30912928-1 2019 Recent studies have suggested that uremic toxins such as indoxyl sulfate (IS) and indole-3-acetic acid (IAA) from the metabolism of the gut microbiota may be involved in the inflammatory signaling pathway in chronic kidney disease (CKD) patients through the activation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor. Indican 57-72 aryl hydrocarbon receptor Homo sapiens 303-306 30912928-1 2019 Recent studies have suggested that uremic toxins such as indoxyl sulfate (IS) and indole-3-acetic acid (IAA) from the metabolism of the gut microbiota may be involved in the inflammatory signaling pathway in chronic kidney disease (CKD) patients through the activation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor. Indican 74-76 aryl hydrocarbon receptor Homo sapiens 276-301 30912928-1 2019 Recent studies have suggested that uremic toxins such as indoxyl sulfate (IS) and indole-3-acetic acid (IAA) from the metabolism of the gut microbiota may be involved in the inflammatory signaling pathway in chronic kidney disease (CKD) patients through the activation of the aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor. Indican 74-76 aryl hydrocarbon receptor Homo sapiens 303-306 30826567-11 2019 CONCLUSIONS: These findings suggest that higher plasma indoxyl sulfate concentration may be involved in CYP3A phenoconversion. Indican 55-70 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 104-109 30826567-12 2019 Dose adjustment of drugs metabolized by CYP3A may be needed in patients with CYP3A5*1 allele and high blood indoxyl sulfate. Indican 108-123 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 40-45 30826567-12 2019 Dose adjustment of drugs metabolized by CYP3A may be needed in patients with CYP3A5*1 allele and high blood indoxyl sulfate. Indican 108-123 cytochrome P450 family 3 subfamily A member 5 Homo sapiens 77-83 30779214-1 2019 BACKGROUND: Indoxyl sulfate (IS) has been reported not only to increase with the severity of impaired renal function, but also possibly to be a factor associated with bone abnormalities linked to fibroblast growth factor-23 (FGF-23) in humans with chronic kidney disease (CKD). Indican 12-27 fibroblast growth factor 23 Homo sapiens 196-223 30639138-7 2019 Moreover, indoxyl sulfate decreased mRNA expression of NTCP, OATP1B3 and CYP7A1 in primary human hepatocytes. Indican 10-25 solute carrier family 10 member 1 Homo sapiens 55-59 30639138-7 2019 Moreover, indoxyl sulfate decreased mRNA expression of NTCP, OATP1B3 and CYP7A1 in primary human hepatocytes. Indican 10-25 solute carrier organic anion transporter family member 1B3 Homo sapiens 61-68 30639138-7 2019 Moreover, indoxyl sulfate decreased mRNA expression of NTCP, OATP1B3 and CYP7A1 in primary human hepatocytes. Indican 10-25 cytochrome P450 family 7 subfamily A member 1 Homo sapiens 73-79 30779214-0 2019 The association of indoxyl sulfate with fibroblast growth factor-23 in cats with chronic kidney disease. Indican 19-34 fibroblast growth factor 23 Felis catus 40-67 30779214-1 2019 BACKGROUND: Indoxyl sulfate (IS) has been reported not only to increase with the severity of impaired renal function, but also possibly to be a factor associated with bone abnormalities linked to fibroblast growth factor-23 (FGF-23) in humans with chronic kidney disease (CKD). Indican 12-27 fibroblast growth factor 23 Homo sapiens 225-231 30779214-1 2019 BACKGROUND: Indoxyl sulfate (IS) has been reported not only to increase with the severity of impaired renal function, but also possibly to be a factor associated with bone abnormalities linked to fibroblast growth factor-23 (FGF-23) in humans with chronic kidney disease (CKD). Indican 29-31 fibroblast growth factor 23 Homo sapiens 196-223 30779214-1 2019 BACKGROUND: Indoxyl sulfate (IS) has been reported not only to increase with the severity of impaired renal function, but also possibly to be a factor associated with bone abnormalities linked to fibroblast growth factor-23 (FGF-23) in humans with chronic kidney disease (CKD). Indican 29-31 fibroblast growth factor 23 Homo sapiens 225-231 30779214-3 2019 HYPOTHESIS: Accumulation of IS is related to FGF-23 secretion in cats with CKD. Indican 8-10 fibroblast growth factor 23 Felis catus 45-51 30779214-8 2019 Higher concentration of FGF-23 was significantly associated with higher concentration of IS after adjusting for various confounding factors including creatinine and phosphate. Indican 89-91 fibroblast growth factor 23 Felis catus 24-30 30692076-6 2019 RESULTS: Rat cardiomyocytes treated with IS showed significantly enhanced protein synthesis and increased expression levels of BNP, p-erk1/2, and p-p38 as compared with the control cells (P &lt; 0.01), but the expression of p-jnk was comparable between the two groups. Indican 41-43 natriuretic peptide B Rattus norvegicus 127-130 30586693-0 2019 Uremic Toxin Indoxyl Sulfate Promotes Proinflammatory Macrophage Activation Via the Interplay of OATP2B1 and Dll4-Notch Signaling. Indican 13-28 delta like canonical Notch ligand 4 Mus musculus 109-113 30586693-9 2019 RESULTS: We found that indoxyl sulfate-induced proinflammatory macrophage activation is mediated by its uptake through transporters, including OATP2B1, encoded by the SLCO2B1 gene. Indican 23-38 solute carrier organic anion transporter family, member 2b1 Mus musculus 167-174 30586693-12 2019 As predicted computationally, indoxyl sulfate triggered Notch signaling, which was preceded by the rapid induction of Dll4 protein. Indican 30-45 delta like canonical Notch ligand 4 Mus musculus 118-122 30586693-14 2019 In mice, macrophage-targeted OATP2B1/Slco2b1 silencing and Dll4 antibody inhibited proinflammatory activation of peritoneal macrophages induced by indoxyl sulfate. Indican 147-162 solute carrier organic anion transporter family, member 2b1 Mus musculus 37-44 30586693-14 2019 In mice, macrophage-targeted OATP2B1/Slco2b1 silencing and Dll4 antibody inhibited proinflammatory activation of peritoneal macrophages induced by indoxyl sulfate. Indican 147-162 delta like canonical Notch ligand 4 Mus musculus 59-63 30586693-16 2019 Moreover, coadministration of indoxyl sulfate and OATP2B1/Slco2b1 or Dll4 siRNA encapsulated in macrophage-targeted lipid nanoparticles in Ldlr-/- mice suppressed lesion development. Indican 30-45 low density lipoprotein receptor Mus musculus 139-143 30586693-17 2019 CONCLUSIONS: These results suggest that novel crosstalk between OATP2B1 and Dll4-Notch signaling in macrophages mediates indoxyl sulfate-induced vascular inflammation in CKD. Indican 121-136 delta like canonical Notch ligand 4 Mus musculus 76-80 31085925-0 2019 Indoxyl Sulfate-Induced Extracellular Vesicles Released from Endothelial Cells Stimulate Vascular Smooth Muscle Cell Proliferation by Inducing Transforming Growth Factor-Beta Production. Indican 0-15 transforming growth factor beta 1 Homo sapiens 143-174 29964132-2 2018 Vancomycin suppressed the mRNA and protein expressions of Oat1, Oat3, Oct2, Mrp2 and P-gp to reduce the renal excretion of endogenous toxins (e.g. indoxyl sulfate). Indican 147-162 solute carrier family 22 member 6 Rattus norvegicus 58-62 30595680-4 2018 In this study, we aimed to evaluate the impact of renal impairment severity-dependent accumulation of indoxyl sulfate on hepatic CYP3A activity using metabolic markers. Indican 102-117 cytochrome P450 family 3 subfamily A member 4 Homo sapiens 129-134 28992684-0 2019 Paricalcitol attenuates indoxyl sulfate-induced apoptosis through the inhibition of MAPK, Akt, and NF-kB activation in HK-2 cells. Indican 24-39 AKT serine/threonine kinase 1 Homo sapiens 90-93 28992684-11 2019 Additionally, flow cytometry analysis revealed that IS-induced apoptosis was attenuated by paricalcitol treatment, which resulted in decreased numbers of fluorescein isothiocyanate-conjugated Annexin V positive cells. Indican 52-54 annexin A5 Homo sapiens 192-201 30546314-0 2018 Indoxyl Sulfate Promotes Arterial Thrombosis in Rat Model via Increased Levels of Complex TF/VII, PAI-1, Platelet Activation as Well as Decreased Contents of SIRT1 and SIRT3. Indican 0-15 serpin family E member 1 Rattus norvegicus 98-103 30546314-0 2018 Indoxyl Sulfate Promotes Arterial Thrombosis in Rat Model via Increased Levels of Complex TF/VII, PAI-1, Platelet Activation as Well as Decreased Contents of SIRT1 and SIRT3. Indican 0-15 sirtuin 1 Rattus norvegicus 158-163 30546314-0 2018 Indoxyl Sulfate Promotes Arterial Thrombosis in Rat Model via Increased Levels of Complex TF/VII, PAI-1, Platelet Activation as Well as Decreased Contents of SIRT1 and SIRT3. Indican 0-15 sirtuin 3 Rattus norvegicus 168-173 30336612-0 2018 AST-120 Reduces Neuroinflammation Induced by Indoxyl Sulfate in Glial Cells. Indican 45-60 solute carrier family 17 member 5 Homo sapiens 0-3 30205954-2 2018 We have previously shown that indoxyl sulfate (IS), a representative protein-bound uremic toxin accumulated in the blood of CKD patients, inhibits hypoxia-induced HIF activation and subsequent EPO production through activation of aryl hydrocarbon receptor (AHR). Indican 30-45 erythropoietin Homo sapiens 193-196 30205954-2 2018 We have previously shown that indoxyl sulfate (IS), a representative protein-bound uremic toxin accumulated in the blood of CKD patients, inhibits hypoxia-induced HIF activation and subsequent EPO production through activation of aryl hydrocarbon receptor (AHR). Indican 30-45 aryl hydrocarbon receptor Homo sapiens 230-255 30205954-2 2018 We have previously shown that indoxyl sulfate (IS), a representative protein-bound uremic toxin accumulated in the blood of CKD patients, inhibits hypoxia-induced HIF activation and subsequent EPO production through activation of aryl hydrocarbon receptor (AHR). Indican 30-45 aryl hydrocarbon receptor Homo sapiens 257-260 29964132-2 2018 Vancomycin suppressed the mRNA and protein expressions of Oat1, Oat3, Oct2, Mrp2 and P-gp to reduce the renal excretion of endogenous toxins (e.g. indoxyl sulfate). Indican 147-162 solute carrier family 22 member 8 Rattus norvegicus 64-68 29964132-2 2018 Vancomycin suppressed the mRNA and protein expressions of Oat1, Oat3, Oct2, Mrp2 and P-gp to reduce the renal excretion of endogenous toxins (e.g. indoxyl sulfate). Indican 147-162 solute carrier family 22 member 2 Rattus norvegicus 70-74 29964132-2 2018 Vancomycin suppressed the mRNA and protein expressions of Oat1, Oat3, Oct2, Mrp2 and P-gp to reduce the renal excretion of endogenous toxins (e.g. indoxyl sulfate). Indican 147-162 ATP binding cassette subfamily C member 2 Rattus norvegicus 76-80 29964132-2 2018 Vancomycin suppressed the mRNA and protein expressions of Oat1, Oat3, Oct2, Mrp2 and P-gp to reduce the renal excretion of endogenous toxins (e.g. indoxyl sulfate). Indican 147-162 ATP-binding cassette, subfamily B (MDR/TAP), member 1B Rattus norvegicus 85-89 29976888-0 2018 Indoxyl Sulfate, a Uremic Toxin, Stimulates Reactive Oxygen Species Production and Erythrocyte Cell Death Supposedly by an Organic Anion Transporter 2 (OAT2) and NADPH Oxidase Activity-Dependent Pathways. Indican 0-15 solute carrier family 22 member 7 Homo sapiens 123-150 30205620-7 2018 PE concentrations of ENA-78/VEGF/IL-8/MDC/PCS/indoxyl sulphate correlate with serum creatinine concentrations. Indican 46-62 C-X-C motif chemokine ligand 5 Homo sapiens 21-27 29864403-6 2018 With an increase in IS, there is a decrease in the osteoblast Wnt/b-catenin signaling and increase in the expression of Wnt signaling inhibitors, such as sclerostin and Dickkopf-1 (DKK1). Indican 20-22 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 169-179 29864403-6 2018 With an increase in IS, there is a decrease in the osteoblast Wnt/b-catenin signaling and increase in the expression of Wnt signaling inhibitors, such as sclerostin and Dickkopf-1 (DKK1). Indican 20-22 dickkopf WNT signaling pathway inhibitor 1 Homo sapiens 181-185 30042379-0 2018 Identification of ABCG2 as an Exporter of Uremic Toxin Indoxyl Sulfate in Mice and as a Crucial Factor Influencing CKD Progression. Indican 55-70 ATP binding cassette subfamily G member 2 (Junior blood group) Mus musculus 18-23 30042379-4 2018 Our results demonstrated that ATP-binding cassette transporter subfamily G member 2 (ABCG2) is a major transporter of the uremic toxin indoxyl sulfate. Indican 135-150 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 85-90 30042379-5 2018 ABCG2 regulates the pathophysiological excretion of indoxyl sulfate and strongly affects CKD survival rates. Indican 52-67 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 0-5 30042379-6 2018 Our study is the first to report ABCG2 as a physiological exporter of indoxyl sulfate and identify ABCG2 as a crucial factor influencing CKD progression, consistent with the observed association between ABCG2 function and age of dialysis onset in humans. Indican 70-85 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 33-38 29976888-0 2018 Indoxyl Sulfate, a Uremic Toxin, Stimulates Reactive Oxygen Species Production and Erythrocyte Cell Death Supposedly by an Organic Anion Transporter 2 (OAT2) and NADPH Oxidase Activity-Dependent Pathways. Indican 0-15 solute carrier family 22 member 7 Homo sapiens 152-156 29703382-2 2018 The major metabolite of indican was indoxyl sulfate (IS), an uremic toxin which was a known substrate/inhibitor of organic anion transporter (OAT) 1, OAT 3 and multidrug resistance-associated protein (MRP) 4. Indican 24-31 solute carrier family 22 member 6 Rattus norvegicus 115-148 29380555-11 2018 Indoxyl sulfate inhibits myoblast proliferation and induces the myotubular atrophy marker atrogin-1 protein expression. Indican 0-15 F-box protein 32 Mus musculus 90-99 29380555-12 2018 Indoxyl sulfate stimulates eIF2alpha phosphorylation and XBP1 mRNA splicing in UPR. Indican 0-15 eukaryotic translation initiation factor 2A Mus musculus 27-36 29380555-12 2018 Indoxyl sulfate stimulates eIF2alpha phosphorylation and XBP1 mRNA splicing in UPR. Indican 0-15 X-box binding protein 1 Mus musculus 57-61 29703382-2 2018 The major metabolite of indican was indoxyl sulfate (IS), an uremic toxin which was a known substrate/inhibitor of organic anion transporter (OAT) 1, OAT 3 and multidrug resistance-associated protein (MRP) 4. Indican 36-51 solute carrier family 22 member 6 Rattus norvegicus 115-148 29703382-4 2018 We hypothesized that IS, the major metabolite of oral indican, might inhibit the renal excretion of MTX mediated by OAT 1, OAT 3 and MRP 4. Indican 54-61 solute carrier family 22 member 6 Rattus norvegicus 116-121 29703382-4 2018 We hypothesized that IS, the major metabolite of oral indican, might inhibit the renal excretion of MTX mediated by OAT 1, OAT 3 and MRP 4. Indican 54-61 solute carrier family 22 member 8 Rattus norvegicus 123-128 29703382-4 2018 We hypothesized that IS, the major metabolite of oral indican, might inhibit the renal excretion of MTX mediated by OAT 1, OAT 3 and MRP 4. Indican 54-61 ATP binding cassette subfamily C member 4 Rattus norvegicus 133-138 29703382-11 2018 In conclusion, oral indican increased the systemic exposure and MRT of MTX through inhibition on multiple anion transporters including OAT 1, OAT 3 and MRP 4 by the major metabolite IS. Indican 20-27 solute carrier family 22 member 6 Rattus norvegicus 135-140 29703382-11 2018 In conclusion, oral indican increased the systemic exposure and MRT of MTX through inhibition on multiple anion transporters including OAT 1, OAT 3 and MRP 4 by the major metabolite IS. Indican 20-27 solute carrier family 22 member 8 Rattus norvegicus 142-147 29703382-11 2018 In conclusion, oral indican increased the systemic exposure and MRT of MTX through inhibition on multiple anion transporters including OAT 1, OAT 3 and MRP 4 by the major metabolite IS. Indican 20-27 ATP binding cassette subfamily C member 4 Rattus norvegicus 152-157 29395338-2 2018 Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AHR). Indican 25-40 aryl hydrocarbon receptor Homo sapiens 83-108 29395338-2 2018 Some uremic toxins, like indoxyl sulfate, are agonists of the transcription factor aryl hydrocarbon receptor (AHR). Indican 25-40 aryl hydrocarbon receptor Homo sapiens 110-113 29395338-10 2018 After serial indoxyl sulfate injections, we observed an increase in serum AHR-AP and in expression of Cyp1a1 mRNA in aorta and heart in WT mice, but not in AhR-/- mice. Indican 13-28 aryl-hydrocarbon receptor Mus musculus 74-77 29395338-6 2018 Compared to sera from healthy controls, sera from CKD patients displayed a strong AHR-Activating Potential; strongly correlated with eGFR and with the indoxyl sulfate concentration. Indican 151-166 aryl hydrocarbon receptor Homo sapiens 82-85 29543732-0 2018 Indoxyl Sulfate Promotes Macrophage IL-1beta Production by Activating Aryl Hydrocarbon Receptor/NF-kappa/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated. Indican 0-15 interleukin 1 beta Homo sapiens 36-44 29395338-10 2018 After serial indoxyl sulfate injections, we observed an increase in serum AHR-AP and in expression of Cyp1a1 mRNA in aorta and heart in WT mice, but not in AhR-/- mice. Indican 13-28 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 102-108 28992067-0 2018 The uremic toxin indoxyl sulfate interferes with iron metabolism by regulating hepcidin in chronic kidney disease. Indican 17-32 hepcidin antimicrobial peptide Mus musculus 79-87 29543732-0 2018 Indoxyl Sulfate Promotes Macrophage IL-1beta Production by Activating Aryl Hydrocarbon Receptor/NF-kappa/MAPK Cascades, but the NLRP3 inflammasome Was Not Activated. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 70-95 29371912-9 2017 Moreover, decreased cell viability induced by IS was shown to be attenuated by IL-1beta or IL-18-neutralizing antibody. Indican 46-48 interleukin 1 beta Rattus norvegicus 79-87 29343519-2 2018 Using mouse models, we recently described indoxyl sulfate, a tryptophan metabolite retained in CKD and an activator of tissue factor (TF) through aryl hydrocarbon receptor (AHR) signaling, as an inducer of thrombosis across the CKD spectrum. Indican 42-57 coagulation factor III Mus musculus 119-132 29343519-2 2018 Using mouse models, we recently described indoxyl sulfate, a tryptophan metabolite retained in CKD and an activator of tissue factor (TF) through aryl hydrocarbon receptor (AHR) signaling, as an inducer of thrombosis across the CKD spectrum. Indican 42-57 coagulation factor III Mus musculus 134-136 29343519-2 2018 Using mouse models, we recently described indoxyl sulfate, a tryptophan metabolite retained in CKD and an activator of tissue factor (TF) through aryl hydrocarbon receptor (AHR) signaling, as an inducer of thrombosis across the CKD spectrum. Indican 42-57 aryl-hydrocarbon receptor Mus musculus 146-171 29343519-2 2018 Using mouse models, we recently described indoxyl sulfate, a tryptophan metabolite retained in CKD and an activator of tissue factor (TF) through aryl hydrocarbon receptor (AHR) signaling, as an inducer of thrombosis across the CKD spectrum. Indican 42-57 aryl-hydrocarbon receptor Mus musculus 173-176 29203210-0 2018 Indoxyl sulfate upregulates the cannabinoid type 1 receptor gene via an ATF3/c-Jun complex-mediated signaling pathway in the model of uremic cardiomyopathy. Indican 0-15 activating transcription factor 3 Homo sapiens 72-76 29203210-0 2018 Indoxyl sulfate upregulates the cannabinoid type 1 receptor gene via an ATF3/c-Jun complex-mediated signaling pathway in the model of uremic cardiomyopathy. Indican 0-15 Jun proto-oncogene, AP-1 transcription factor subunit Homo sapiens 77-82 29222397-0 2018 Indoxyl Sulfate Upregulates Liver P-Glycoprotein Expression and Activity through Aryl Hydrocarbon Receptor Signaling. Indican 0-15 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 29222397-0 2018 Indoxyl Sulfate Upregulates Liver P-Glycoprotein Expression and Activity through Aryl Hydrocarbon Receptor Signaling. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 81-106 29195902-0 2018 Indoxyl sulfate accelerates vascular smooth muscle cell calcification via microRNA-29b dependent regulation of Wnt/beta-catenin signaling. Indican 0-15 catenin beta 1 Homo sapiens 115-127 29511436-0 2018 Dihydroartemisinin inhibits indoxyl sulfate (IS)-promoted cell cycle progression in mesangial cells by targeting COX-2/mPGES-1/PGE2 cascade. Indican 28-43 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118 29511436-0 2018 Dihydroartemisinin inhibits indoxyl sulfate (IS)-promoted cell cycle progression in mesangial cells by targeting COX-2/mPGES-1/PGE2 cascade. Indican 28-43 prostaglandin E synthase Mus musculus 119-126 29511436-0 2018 Dihydroartemisinin inhibits indoxyl sulfate (IS)-promoted cell cycle progression in mesangial cells by targeting COX-2/mPGES-1/PGE2 cascade. Indican 45-47 mitochondrially encoded cytochrome c oxidase II Homo sapiens 113-118 29511436-0 2018 Dihydroartemisinin inhibits indoxyl sulfate (IS)-promoted cell cycle progression in mesangial cells by targeting COX-2/mPGES-1/PGE2 cascade. Indican 45-47 prostaglandin E synthase Mus musculus 119-126 29371912-9 2017 Moreover, decreased cell viability induced by IS was shown to be attenuated by IL-1beta or IL-18-neutralizing antibody. Indican 46-48 interleukin 18 Rattus norvegicus 91-96 29238104-6 2017 The effects of IPA on IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 were studied using proximal tubular cells (HK-2). Indican 22-24 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 52-58 28887287-7 2017 Uptake of simvastatin acid was significantly increased by known (benzylpenicillin and estrone-3-sulfate) and potential (indoxyl sulfate and cyclosporine) substrates of OATP3A1. Indican 120-135 solute carrier organic anion transporter family member 3A1 Homo sapiens 168-175 29107962-2 2017 In this study, we sought to determine if Apoptosis Signal-Regulated Kinase 1 (ASK1), an upstream regulator of cellular stress response, mediates cardiac hypertrophy and cardiorenal fibrosis induced by indoxyl sulfate (IS) and p-cresol sulfate (PCS) in vitro, and whether ASK1 inhibition is beneficial to ameliorate these cellular effects. Indican 201-216 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 41-76 29107962-2 2017 In this study, we sought to determine if Apoptosis Signal-Regulated Kinase 1 (ASK1), an upstream regulator of cellular stress response, mediates cardiac hypertrophy and cardiorenal fibrosis induced by indoxyl sulfate (IS) and p-cresol sulfate (PCS) in vitro, and whether ASK1 inhibition is beneficial to ameliorate these cellular effects. Indican 201-216 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 78-82 29107962-2 2017 In this study, we sought to determine if Apoptosis Signal-Regulated Kinase 1 (ASK1), an upstream regulator of cellular stress response, mediates cardiac hypertrophy and cardiorenal fibrosis induced by indoxyl sulfate (IS) and p-cresol sulfate (PCS) in vitro, and whether ASK1 inhibition is beneficial to ameliorate these cellular effects. Indican 218-220 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 41-76 29107962-2 2017 In this study, we sought to determine if Apoptosis Signal-Regulated Kinase 1 (ASK1), an upstream regulator of cellular stress response, mediates cardiac hypertrophy and cardiorenal fibrosis induced by indoxyl sulfate (IS) and p-cresol sulfate (PCS) in vitro, and whether ASK1 inhibition is beneficial to ameliorate these cellular effects. Indican 218-220 mitogen-activated protein kinase kinase kinase 5 Homo sapiens 78-82 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 0-15 transforming growth factor, beta 1 Mus musculus 112-144 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 17-19 transforming growth factor, beta 1 Mus musculus 146-155 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 0-15 transforming growth factor, beta 1 Mus musculus 146-155 29238104-6 2017 The effects of IPA on IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 were studied using proximal tubular cells (HK-2). Indican 22-24 transforming growth factor, beta 1 Mus musculus 60-69 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 0-15 chemokine (C-C motif) ligand 2 Mus musculus 161-191 29238104-6 2017 The effects of IPA on IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 were studied using proximal tubular cells (HK-2). Indican 22-24 chemokine (C-C motif) ligand 2 Mus musculus 75-80 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 0-15 chemokine (C-C motif) ligand 2 Mus musculus 193-198 29238104-12 2017 In conclusion, IPA suppressed the IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 through suppression of Stat3 in proximal tubular cells. Indican 34-36 aryl-hydrocarbon receptor Mus musculus 59-62 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 17-19 transforming growth factor, beta 1 Mus musculus 112-144 29238104-12 2017 In conclusion, IPA suppressed the IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 through suppression of Stat3 in proximal tubular cells. Indican 34-36 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 64-70 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 17-19 chemokine (C-C motif) ligand 2 Mus musculus 161-191 29238104-12 2017 In conclusion, IPA suppressed the IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 through suppression of Stat3 in proximal tubular cells. Indican 34-36 transforming growth factor, beta 1 Mus musculus 72-81 29238104-1 2017 Indoxyl sulfate (IS) induces fibrosis and inflammation in kidneys via oxidative stress through the induction of transforming growth factor-beta1 (TGF-beta1) and monocyte chemotactic protein-1 (MCP-1). Indican 17-19 chemokine (C-C motif) ligand 2 Mus musculus 193-198 29238104-6 2017 The effects of IPA on IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 were studied using proximal tubular cells (HK-2). Indican 22-24 aryl-hydrocarbon receptor Mus musculus 47-50 29238104-12 2017 In conclusion, IPA suppressed the IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 through suppression of Stat3 in proximal tubular cells. Indican 34-36 chemokine (C-C motif) ligand 2 Mus musculus 87-92 29238104-12 2017 In conclusion, IPA suppressed the IS-induced expression of AHR, CYP1A1, TGF-beta1, and MCP-1 through suppression of Stat3 in proximal tubular cells. Indican 34-36 signal transducer and activator of transcription 3 Mus musculus 116-121 32095460-1 2017 Indoxyl sulfate, a protein-bound uremic toxin, leads to CKD (chronic kidney disease) progression and its complications through the activation of AhR (aryl hydrocarbon receptor) and RAS (renin-angiotensin system). Indican 0-15 aryl hydrocarbon receptor Homo sapiens 150-175 32095460-0 2017 Inhibition of indoxyl sulfate-induced intrarenal renin-angiotensin system activation: targeting the aryl hydrocarbon receptor. Indican 14-29 aryl hydrocarbon receptor Homo sapiens 100-125 28791957-4 2017 Evaluation of the mechanisms that underlie the high reactivity of indoxyl sulfate and its biological effects showed that this compound is an agonist of the aryl hydrocarbon receptor (AhR). Indican 66-81 aryl hydrocarbon receptor Homo sapiens 156-181 32095460-1 2017 Indoxyl sulfate, a protein-bound uremic toxin, leads to CKD (chronic kidney disease) progression and its complications through the activation of AhR (aryl hydrocarbon receptor) and RAS (renin-angiotensin system). Indican 0-15 aryl hydrocarbon receptor Homo sapiens 145-148 28791957-4 2017 Evaluation of the mechanisms that underlie the high reactivity of indoxyl sulfate and its biological effects showed that this compound is an agonist of the aryl hydrocarbon receptor (AhR). Indican 66-81 aryl hydrocarbon receptor Homo sapiens 183-186 28791957-6 2017 The following paper describes the role of indoxyl sulfate as AhR ligand in the context of the excessive accumulation, which appears as one of the symptoms associated with chronic kidney disease. Indican 42-57 aryl hydrocarbon receptor Homo sapiens 61-64 28508124-0 2017 DNA hypermethylation of sFRP5 contributes to indoxyl sulfate-induced renal fibrosis. Indican 45-60 secreted frizzled related protein 5 Homo sapiens 24-29 29137321-2 2017 In vitro studies have shown that indoxyl sulfate decreases erythropoietin production. Indican 33-48 erythropoietin Homo sapiens 59-73 29137321-5 2017 We found serum indoxyl sulfate levels are significantly and negatively associated with erythropoietin levels in human. Indican 15-30 erythropoietin Homo sapiens 87-101 29137321-6 2017 A multiple stepwise linear regression analyses after adjustment for other independent parameters revealed that free indoxyl sulfate, and total indoxyl sulfate were significantly associated with erythropoietin levels. Indican 116-131 erythropoietin Homo sapiens 194-208 29137321-6 2017 A multiple stepwise linear regression analyses after adjustment for other independent parameters revealed that free indoxyl sulfate, and total indoxyl sulfate were significantly associated with erythropoietin levels. Indican 143-158 erythropoietin Homo sapiens 194-208 29137321-7 2017 In animal studies, erythropoietin gene and protein expression were markedly inhibited in rats with chronic kidney disease; however, this effect was significantly reversed by lowering serum indoxyl sulfate with AST-120. Indican 189-204 erythropoietin Rattus norvegicus 19-33 29137321-8 2017 Indoxyl sulfate may also inhibit erythropoietin expression in animal models with chronic kidney disease. Indican 0-15 erythropoietin Homo sapiens 33-47 28508124-2 2017 In this study, we first showed that the progress of renal fibrosis was positively related to serum levels of indoxyl sulfate, a typical protein-bound toxin, and that there was a close correlation between serum indoxyl sulfate levels and beta-catenin expression in the kidneys (r = 0.908, p < 0.001) of CKD patients. Indican 210-225 catenin beta 1 Homo sapiens 237-249 28508124-3 2017 We then demonstrated that intraperitoneal injections of indoxyl sulfate (100 mg/kg/day) for 4 weeks in uninephrectomized mice explicitly induced renal fibrosis, which was accompanied by a significant activation of Wnt/beta-catenin signaling. Indican 56-71 catenin (cadherin associated protein), beta 1 Mus musculus 218-230 28508124-4 2017 In vitro investigations in human renal tubular HK-2 cells revealed that indoxyl sulfate exhibited a potent ability to induce Wnt/beta-catenin activation through the downregulation of sFRP5, a gene that codes for an extracellular antagonist of Wnt signaling, by increasing the DNA methylation level of its promoter CpG islands. Indican 72-87 catenin beta 1 Homo sapiens 129-141 28508124-4 2017 In vitro investigations in human renal tubular HK-2 cells revealed that indoxyl sulfate exhibited a potent ability to induce Wnt/beta-catenin activation through the downregulation of sFRP5, a gene that codes for an extracellular antagonist of Wnt signaling, by increasing the DNA methylation level of its promoter CpG islands. Indican 72-87 secreted frizzled related protein 5 Homo sapiens 183-188 28508124-5 2017 The increased expression of DNA methyltransferases following the activation of ROS/ERK1/2 signaling was responsible for the DNA hypermethylation of sFRP5 induced by indoxyl sulfate. Indican 165-180 mitogen-activated protein kinase 3 Homo sapiens 83-89 28508124-5 2017 The increased expression of DNA methyltransferases following the activation of ROS/ERK1/2 signaling was responsible for the DNA hypermethylation of sFRP5 induced by indoxyl sulfate. Indican 165-180 secreted frizzled related protein 5 Homo sapiens 148-153 28508124-6 2017 Conversely, treatment with 5-aza-2"-deoxycytidine, an inhibitor of DNA methyltransferases, significantly reduced indoxyl sulfate-induced sFRP5 downregulation and Wnt/beta-catenin activation. Indican 113-128 secreted frizzled related protein 5 Homo sapiens 137-142 28508124-6 2017 Conversely, treatment with 5-aza-2"-deoxycytidine, an inhibitor of DNA methyltransferases, significantly reduced indoxyl sulfate-induced sFRP5 downregulation and Wnt/beta-catenin activation. Indican 113-128 catenin beta 1 Homo sapiens 166-178 28508124-7 2017 In vivo, intraperitoneal injections of recombinant sFRP5 protein or 5-aza-2"-deoxycytidine substantially alleviated renal fibrosis in indoxyl sulfate-treated uninephrectomized mice. Indican 134-149 secreted frizzled-related sequence protein 5 Mus musculus 51-56 28508124-8 2017 Our results suggest that indoxyl sulfate promotes renal fibrosis through the induction of DNA hypermethylation of sFRP5, and thereafter the activation of Wnt/beta-catenin signaling. Indican 25-40 secreted frizzled related protein 5 Homo sapiens 114-119 28508124-8 2017 Our results suggest that indoxyl sulfate promotes renal fibrosis through the induction of DNA hypermethylation of sFRP5, and thereafter the activation of Wnt/beta-catenin signaling. Indican 25-40 catenin beta 1 Homo sapiens 158-170 28277985-0 2017 Indoxyl sulfate potentiates endothelial dysfunction via reciprocal role for reactive oxygen species and RhoA/ROCK signaling in 5/6 nephrectomized rats. Indican 0-15 ras homolog family member A Rattus norvegicus 104-108 28185988-3 2017 The renal excretion of IS was mediated by organic anion transporters (OATs) OAT 1 and OAT 3. Indican 23-25 solute carrier family 22 member 6 Rattus norvegicus 76-81 28185988-3 2017 The renal excretion of IS was mediated by organic anion transporters (OATs) OAT 1 and OAT 3. Indican 23-25 solute carrier family 22 member 8 Rattus norvegicus 86-91 27990791-2 2017 Indoxyl sulfate induces cellular dysfunction by producing reactive oxygen species (ROS) such as superoxide by activating nicotinamide adenine dinucleotide phosphate oxidase, and by activating aryl hydrocarbon receptor through its uptake via organic anion transporters (OAT1 and OAT3). Indican 0-15 aryl hydrocarbon receptor Homo sapiens 192-217 27990791-2 2017 Indoxyl sulfate induces cellular dysfunction by producing reactive oxygen species (ROS) such as superoxide by activating nicotinamide adenine dinucleotide phosphate oxidase, and by activating aryl hydrocarbon receptor through its uptake via organic anion transporters (OAT1 and OAT3). Indican 0-15 potassium two pore domain channel subfamily K member 3 Homo sapiens 269-273 27990791-2 2017 Indoxyl sulfate induces cellular dysfunction by producing reactive oxygen species (ROS) such as superoxide by activating nicotinamide adenine dinucleotide phosphate oxidase, and by activating aryl hydrocarbon receptor through its uptake via organic anion transporters (OAT1 and OAT3). Indican 0-15 solute carrier family 22 member 8 Homo sapiens 278-282 27990791-5 2017 The carbon adsorbent AST-120 might be useful to delay the progression of not only CKD but also CVD, osteodystrophy, and sarcopenia by adsorbing its precursor, indole, in the intestines, and consequently reducing the serum levels of indoxyl sulfate. Indican 232-247 solute carrier family 17 member 5 Homo sapiens 21-24 28277985-1 2017 Accumulative indoxyl sulfate (IS) retained in chronic kidney disease (CKD) can potentiate vascular endothelial dysfunction, and herein, we aim at elucidating the underlying mechanisms from the perspective of possible association between reactive oxygen species (ROS) and RhoA/ROCK pathway. Indican 13-28 ras homolog family member A Rattus norvegicus 271-275 28025487-0 2016 Indoxyl Sulfate as a Mediator Involved in Dysregulation of Pulmonary Aquaporin-5 in Acute Lung Injury Caused by Acute Kidney Injury. Indican 0-15 aquaporin 5 Rattus norvegicus 69-80 28392999-7 2017 At one year, the AST-120-induced decrease in the serum indoxyl sulfate concentration inversely correlated with the occurrence of composite primary outcomes: second tertile HR 1.59, 95% CI 0.82 to 3.07, P = 0.17; third tertile HR 2.11, 95% CI 1.07 to 4.17, P = 0.031. Indican 55-70 solute carrier family 17 member 5 Homo sapiens 17-20 28392999-10 2017 Reduction of the serum indoxyl sulfate level may be used to identify patients who would benefit from AST-120 administration. Indican 23-38 solute carrier family 17 member 5 Homo sapiens 101-104 28490014-2 2017 Uremic toxins such as indoxyl sulfate and indole acetic acid are derived from tryptophan fermentation by gut microbiota; they accumulate in patients with chronic kidney disease (CKD) on haemodialysis and have recently emerged as potent ligands of AhR. Indican 22-37 aryl hydrocarbon receptor Homo sapiens 247-250 28854439-0 2017 mPGES-1-Derived PGE2 Contributes to Indoxyl Sulfate-Induced Mesangial Cell Proliferation. Indican 36-51 prostaglandin E synthase Mus musculus 0-7 27001263-0 2016 Indoxyl sulfate promotes vascular smooth muscle cell calcification via the JNK/Pit-1 pathway. Indican 0-15 mitogen-activated protein kinase 8 Homo sapiens 75-78 27830716-5 2016 Comprehensive metabolomics revealed that indoxyl sulfate induces metabolic alterations such as upregulation of glycolysis, including pentose phosphate pathway acceleration as antioxidative stress response, via nuclear factor (erythroid-2-related factor)-2. Indican 41-56 NFE2 like bZIP transcription factor 2 Homo sapiens 210-255 26659566-0 2016 Indoxyl sulfate enhances IL-1beta-induced E-selectin expression in endothelial cells in acute kidney injury by the ROS/MAPKs/NFkappaB/AP-1 pathway. Indican 0-15 interleukin 1 beta Homo sapiens 25-33 26659566-0 2016 Indoxyl sulfate enhances IL-1beta-induced E-selectin expression in endothelial cells in acute kidney injury by the ROS/MAPKs/NFkappaB/AP-1 pathway. Indican 0-15 selectin E Homo sapiens 42-52 26659566-0 2016 Indoxyl sulfate enhances IL-1beta-induced E-selectin expression in endothelial cells in acute kidney injury by the ROS/MAPKs/NFkappaB/AP-1 pathway. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 125-133 26659566-0 2016 Indoxyl sulfate enhances IL-1beta-induced E-selectin expression in endothelial cells in acute kidney injury by the ROS/MAPKs/NFkappaB/AP-1 pathway. Indican 0-15 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 134-138 27550174-0 2016 Novel regulations of MEF2-A, MEF2-D, and CACNA1S in the functional incompetence of adipose-derived mesenchymal stem cells by induced indoxyl sulfate in chronic kidney disease. Indican 133-148 myocyte enhancer factor 2A Homo sapiens 21-27 27550174-0 2016 Novel regulations of MEF2-A, MEF2-D, and CACNA1S in the functional incompetence of adipose-derived mesenchymal stem cells by induced indoxyl sulfate in chronic kidney disease. Indican 133-148 calcium voltage-gated channel subunit alpha1 S Homo sapiens 41-48 27550174-8 2016 Moreover, MEF2-A, MEF2-D and CACNA1S expression significantly decreased after indoxyl sulfate treatment. Indican 78-93 myocyte enhancer factor 2A Homo sapiens 10-16 27550174-8 2016 Moreover, MEF2-A, MEF2-D and CACNA1S expression significantly decreased after indoxyl sulfate treatment. Indican 78-93 myocyte enhancer factor 2D Homo sapiens 18-24 27550174-8 2016 Moreover, MEF2-A, MEF2-D and CACNA1S expression significantly decreased after indoxyl sulfate treatment. Indican 78-93 calcium voltage-gated channel subunit alpha1 S Homo sapiens 29-36 26659566-2 2016 In the present study, in cardiovascular surgery-related AKI patients, who are known to have high plasma levels of the uremic toxin indoxyl sulfate (IS), plasma levels of IL-1beta were found to be positively correlated with plasma levels of the adhesion molecule E-selectin. Indican 131-146 interleukin 1 beta Homo sapiens 170-178 27001263-0 2016 Indoxyl sulfate promotes vascular smooth muscle cell calcification via the JNK/Pit-1 pathway. Indican 0-15 POU class 1 homeobox 1 Homo sapiens 79-84 27486223-7 2016 In contrast, the human AHR retains the ancestral sensitivity observed in primates to nontoxic endogenous AHR ligands (e.g., indole, indoxyl sulfate). Indican 132-147 aryl hydrocarbon receptor Homo sapiens 23-26 27486223-7 2016 In contrast, the human AHR retains the ancestral sensitivity observed in primates to nontoxic endogenous AHR ligands (e.g., indole, indoxyl sulfate). Indican 132-147 aryl hydrocarbon receptor Homo sapiens 105-108 26880447-5 2016 shows that indoxyl sulfate suppresses neovascularization in uremic mice by impairing endothelial progenitor cell function via the inhibition of hypoxia-induced hypoxia-inducible factor/interleukin-10/vascular endothelial growth factor signaling. Indican 11-26 interleukin 10 Mus musculus 185-199 26567049-0 2016 Upregulation of nuclear factor-kappaB activity mediates CYP24 expression and reactive oxygen species production in indoxyl sulfate-induced chronic kidney disease. Indican 115-130 nuclear factor kappa B subunit 1 Homo sapiens 16-37 27549031-0 2016 Indoxyl sulfate potentiates skeletal muscle atrophy by inducing the oxidative stress-mediated expression of myostatin and atrogin-1. Indican 0-15 myostatin Mus musculus 108-117 27549031-0 2016 Indoxyl sulfate potentiates skeletal muscle atrophy by inducing the oxidative stress-mediated expression of myostatin and atrogin-1. Indican 0-15 F-box protein 32 Mus musculus 122-131 26860885-0 2016 Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation. Indican 55-70 aryl-hydrocarbon receptor Mus musculus 20-45 26860885-0 2016 Crucial Role of the Aryl Hydrocarbon Receptor (AhR) in Indoxyl Sulfate-Induced Vascular Inflammation. Indican 55-70 aryl-hydrocarbon receptor Mus musculus 47-50 26860885-2 2016 Indoxyl sulfate, a uremic toxin, is associated with cardiovascular disease in patients with chronic kidney disease and has been shown to be a ligand for AhR. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 153-156 26860885-3 2016 The aim of this study was to investigate the potential role of AhR in indoxyl sulfate-induced leukocyte-endothelial interactions. Indican 70-85 aryl-hydrocarbon receptor Mus musculus 63-66 26860885-8 2016 RESULTS: Indoxyl sulfate dramatically enhanced TNF-alpha-induced leukocyte recruitment to the vascular wall in control animals but not in eAhR KO mice. Indican 9-24 tumor necrosis factor Mus musculus 47-56 26860885-10 2016 A luciferase assay revealed that the region between -153 and -146 bps in the E-selectin promoter was responsible for indoxyl sulfate activity via AhR. Indican 117-132 selectin, endothelial cell Mus musculus 77-87 26860885-10 2016 A luciferase assay revealed that the region between -153 and -146 bps in the E-selectin promoter was responsible for indoxyl sulfate activity via AhR. Indican 117-132 aryl-hydrocarbon receptor Mus musculus 146-149 26860885-11 2016 Mutational analysis of this region revealed that activator protein-1 (AP-1) is responsible for indoxyl sulfate-triggered E-selectin expression via AhR. Indican 95-110 jun proto-oncogene Mus musculus 49-68 26860885-11 2016 Mutational analysis of this region revealed that activator protein-1 (AP-1) is responsible for indoxyl sulfate-triggered E-selectin expression via AhR. Indican 95-110 jun proto-oncogene Mus musculus 70-74 26860885-11 2016 Mutational analysis of this region revealed that activator protein-1 (AP-1) is responsible for indoxyl sulfate-triggered E-selectin expression via AhR. Indican 95-110 selectin, endothelial cell Mus musculus 121-131 26860885-11 2016 Mutational analysis of this region revealed that activator protein-1 (AP-1) is responsible for indoxyl sulfate-triggered E-selectin expression via AhR. Indican 95-110 aryl-hydrocarbon receptor Mus musculus 147-150 26860885-12 2016 CONCLUSION: AhR mediates indoxyl sulfate-enhanced leukocyte-endothelial interactions through AP-1 transcriptional activity, which may constitute a new mechanism of vascular inflammation in patients with renal disease. Indican 25-40 aryl hydrocarbon receptor Homo sapiens 12-15 26860885-12 2016 CONCLUSION: AhR mediates indoxyl sulfate-enhanced leukocyte-endothelial interactions through AP-1 transcriptional activity, which may constitute a new mechanism of vascular inflammation in patients with renal disease. Indican 25-40 JunB proto-oncogene, AP-1 transcription factor subunit Homo sapiens 93-97 27766038-0 2016 Indoxyl Sulfate Enhance the Hypermethylation of Klotho and Promote the Process of Vascular Calcification in Chronic Kidney Disease. Indican 0-15 klotho Homo sapiens 48-54 27766038-6 2016 The expression of DNA methyltransferase (DNMT) 1 and 3a in HASMCs treated with IS was significantly increased and specific inhibition of DNA methyltransferase 1 by 5-aza-2"-deoxycytidine(5Aza-2dc) caused demethylation of the Klotho gene and increased Klotho expression. Indican 79-81 DNA methyltransferase 1 Homo sapiens 18-54 27766038-6 2016 The expression of DNA methyltransferase (DNMT) 1 and 3a in HASMCs treated with IS was significantly increased and specific inhibition of DNA methyltransferase 1 by 5-aza-2"-deoxycytidine(5Aza-2dc) caused demethylation of the Klotho gene and increased Klotho expression. Indican 79-81 DNA methyltransferase 1 Homo sapiens 137-160 27766038-6 2016 The expression of DNA methyltransferase (DNMT) 1 and 3a in HASMCs treated with IS was significantly increased and specific inhibition of DNA methyltransferase 1 by 5-aza-2"-deoxycytidine(5Aza-2dc) caused demethylation of the Klotho gene and increased Klotho expression. Indican 79-81 klotho Homo sapiens 225-231 27766038-6 2016 The expression of DNA methyltransferase (DNMT) 1 and 3a in HASMCs treated with IS was significantly increased and specific inhibition of DNA methyltransferase 1 by 5-aza-2"-deoxycytidine(5Aza-2dc) caused demethylation of the Klotho gene and increased Klotho expression. Indican 79-81 klotho Homo sapiens 251-257 26880454-9 2016 In cultured human EPCs, VEGF expression was increased in hypoxia through HIF-1alpha and interleukin-10/STAT3 signaling; effects suppressed by pretreatment with indoxyl sulfate. Indican 160-175 vascular endothelial growth factor A Homo sapiens 24-28 26880454-9 2016 In cultured human EPCs, VEGF expression was increased in hypoxia through HIF-1alpha and interleukin-10/STAT3 signaling; effects suppressed by pretreatment with indoxyl sulfate. Indican 160-175 hypoxia inducible factor 1 subunit alpha Homo sapiens 73-83 26880454-9 2016 In cultured human EPCs, VEGF expression was increased in hypoxia through HIF-1alpha and interleukin-10/STAT3 signaling; effects suppressed by pretreatment with indoxyl sulfate. Indican 160-175 interleukin 10 Homo sapiens 88-102 26880454-9 2016 In cultured human EPCs, VEGF expression was increased in hypoxia through HIF-1alpha and interleukin-10/STAT3 signaling; effects suppressed by pretreatment with indoxyl sulfate. Indican 160-175 signal transducer and activator of transcription 3 Homo sapiens 103-108 26561638-0 2016 Activation of aryl hydrocarbon receptor mediates suppression of hypoxia-inducible factor-dependent erythropoietin expression by indoxyl sulfate. Indican 128-143 aryl hydrocarbon receptor Homo sapiens 14-39 26561638-0 2016 Activation of aryl hydrocarbon receptor mediates suppression of hypoxia-inducible factor-dependent erythropoietin expression by indoxyl sulfate. Indican 128-143 erythropoietin Homo sapiens 99-113 26561638-5 2016 IS also induced AhR activation, and AhR blockade resulted in abolishment of IS-induced suppression of HIF activation. Indican 0-2 aryl hydrocarbon receptor Homo sapiens 16-19 26019318-2 2016 We recently demonstrated that indoxyl sulfate (IS) is a potent CKD-specific prothrombotic metabolite that induces tissue factor (TF) in vascular smooth muscle cells (vSMCs), although the precise mechanism and treatment implications remain unclear. Indican 30-45 coagulation factor III, tissue factor Homo sapiens 114-127 26824459-11 2016 Additionally, their ability to stimulate CD4+CD25+FoxP3+ regulatory T cell production was compromised when hUC-MSCs were pretreated with indoxyl sulfate. Indican 137-152 CD4 molecule Homo sapiens 41-44 26824459-11 2016 Additionally, their ability to stimulate CD4+CD25+FoxP3+ regulatory T cell production was compromised when hUC-MSCs were pretreated with indoxyl sulfate. Indican 137-152 forkhead box P3 Homo sapiens 50-55 26019318-2 2016 We recently demonstrated that indoxyl sulfate (IS) is a potent CKD-specific prothrombotic metabolite that induces tissue factor (TF) in vascular smooth muscle cells (vSMCs), although the precise mechanism and treatment implications remain unclear. Indican 30-45 coagulation factor III, tissue factor Homo sapiens 129-131 26019318-2 2016 We recently demonstrated that indoxyl sulfate (IS) is a potent CKD-specific prothrombotic metabolite that induces tissue factor (TF) in vascular smooth muscle cells (vSMCs), although the precise mechanism and treatment implications remain unclear. Indican 47-49 coagulation factor III, tissue factor Homo sapiens 114-127 26019318-2 2016 We recently demonstrated that indoxyl sulfate (IS) is a potent CKD-specific prothrombotic metabolite that induces tissue factor (TF) in vascular smooth muscle cells (vSMCs), although the precise mechanism and treatment implications remain unclear. Indican 47-49 coagulation factor III, tissue factor Homo sapiens 129-131 27352232-0 2016 Indoxyl Sulfate Downregulates Mas Receptor via Aryl Hydrocarbon Receptor/Nuclear Factor-kappa B, and Induces Cell Proliferation and Tissue Factor Expression in Vascular Smooth Muscle Cells. Indican 0-15 aryl hydrocarbon receptor Rattus norvegicus 47-72 27843201-0 2016 Indoxyl Sulfate Induces Mesangial Cell Proliferation via the Induction of COX-2. Indican 0-15 mitochondrially encoded cytochrome c oxidase II Homo sapiens 74-79 27843201-6 2016 Next, we found an inducible inflammation-related enzyme COX-2 was remarkably enhanced by IS, and the inhibition of COX-2 by NS398 significantly blocked IS-induced MC proliferation in line with a blockade of PGE2 production. Indican 89-91 mitochondrially encoded cytochrome c oxidase II Homo sapiens 56-61 27352232-0 2016 Indoxyl Sulfate Downregulates Mas Receptor via Aryl Hydrocarbon Receptor/Nuclear Factor-kappa B, and Induces Cell Proliferation and Tissue Factor Expression in Vascular Smooth Muscle Cells. Indican 0-15 coagulation factor III, tissue factor Rattus norvegicus 132-145 26408929-0 2015 Deleterious vascular effects of indoxyl sulfate and reversal by oral adsorbent AST-120. Indican 32-47 transmembrane protease, serine 11d Mus musculus 79-82 26552961-3 2015 The renal excretions of IS and PCS were mediated by organic anion transporters (OATs) such as OAT1 and OAT3. Indican 24-26 solute carrier family 22 member 6 Rattus norvegicus 94-98 26552961-3 2015 The renal excretions of IS and PCS were mediated by organic anion transporters (OATs) such as OAT1 and OAT3. Indican 24-26 solute carrier family 22 member 8 Rattus norvegicus 103-107 26408929-3 2015 DESIGN: We studied acute and longer-term effects of IS and AST-120, an oral charcoal adsorbent, on vascular reactivity, endothelium integrity and expression of adhesion molecules VCAM-1 and ICAM-1 in aortic rings of normal and uremic wild type (WT) mice in vitro, and the cardiovascular effects of AST-120 in both WT and apoE-/- mice with CKD in vivo. Indican 52-54 intercellular adhesion molecule 1 Mus musculus 190-196 26287243-0 2015 Increased Proinflammatory Cytokine Production and Decreased Cholesterol Efflux Due to Downregulation of ABCG1 in Macrophages Exposed to Indoxyl Sulfate. Indican 136-151 ATP binding cassette subfamily G member 1 Homo sapiens 104-109 26209659-6 2015 Risk factors of early suppression of 3-IS levels were the type of GI decontamination (P = .01), early onset of antibiotic treatment (P = .001), and recipient NOD2/CARD15 genotype (P = .04). Indican 37-41 nucleotide binding oligomerization domain containing 2 Homo sapiens 158-162 26209659-6 2015 Risk factors of early suppression of 3-IS levels were the type of GI decontamination (P = .01), early onset of antibiotic treatment (P = .001), and recipient NOD2/CARD15 genotype (P = .04). Indican 37-41 nucleotide binding oligomerization domain containing 2 Homo sapiens 163-169 25804281-0 2015 Klotho Protects Against Indoxyl Sulphate-Induced Myocardial Hypertrophy. Indican 24-40 klotho Homo sapiens 0-6 25804281-4 2015 In a survey of 86 patients with CKD, a negative relationship was found between serum levels of IS and Klotho (r=-0.59, P<0.001). Indican 95-97 klotho Homo sapiens 102-108 25804281-5 2015 Furthermore, serum levels of IS and Klotho were independently associated with LVH (for IS: r=0.69, P<0.001; for Klotho: r=-0.49, P<0.001). Indican 29-31 klotho Mus musculus 115-121 25804281-8 2015 In vitro, treatment with Klotho strongly inhibited IS-induced cardiomyocyte hypertrophy by blocking oxidative stress and inhibiting p38 and extracellular signal-regulated protein kinase 1/2 signaling pathways. Indican 51-53 klotho Mus musculus 25-31 25804281-8 2015 In vitro, treatment with Klotho strongly inhibited IS-induced cardiomyocyte hypertrophy by blocking oxidative stress and inhibiting p38 and extracellular signal-regulated protein kinase 1/2 signaling pathways. Indican 51-53 mitogen-activated protein kinase 14 Mus musculus 132-135 26068716-0 2015 Indoxyl sulfate suppresses hepatic fetuin-A expression via the aryl hydrocarbon receptor in HepG2 cells. Indican 0-15 alpha 2-HS glycoprotein Homo sapiens 35-43 26068716-0 2015 Indoxyl sulfate suppresses hepatic fetuin-A expression via the aryl hydrocarbon receptor in HepG2 cells. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 63-88 26277392-0 2015 Nitration of indoxyl sulfate facilitates its cytotoxicity in human renal proximal tubular cells via expression of heme oxygenase-1. Indican 13-28 heme oxygenase 1 Homo sapiens 114-130 26208844-7 2015 The uric acid-, indoxyl sulfate-, and methylguanidine-depolarized RVLM neurons showed the presence of urate transporter 1 (URAT 1), organic anion transporter (OAT)1 or OAT3, and organic cation transporter (OCT)3, respectively. Indican 16-31 solute carrier family 22 member 12 Homo sapiens 102-121 26208844-7 2015 The uric acid-, indoxyl sulfate-, and methylguanidine-depolarized RVLM neurons showed the presence of urate transporter 1 (URAT 1), organic anion transporter (OAT)1 or OAT3, and organic cation transporter (OCT)3, respectively. Indican 16-31 solute carrier family 22 member 12 Homo sapiens 123-129 26208844-7 2015 The uric acid-, indoxyl sulfate-, and methylguanidine-depolarized RVLM neurons showed the presence of urate transporter 1 (URAT 1), organic anion transporter (OAT)1 or OAT3, and organic cation transporter (OCT)3, respectively. Indican 16-31 solute carrier family 22 member 6 Homo sapiens 132-164 26208844-7 2015 The uric acid-, indoxyl sulfate-, and methylguanidine-depolarized RVLM neurons showed the presence of urate transporter 1 (URAT 1), organic anion transporter (OAT)1 or OAT3, and organic cation transporter (OCT)3, respectively. Indican 16-31 solute carrier family 22 member 8 Homo sapiens 168-172 26208844-7 2015 The uric acid-, indoxyl sulfate-, and methylguanidine-depolarized RVLM neurons showed the presence of urate transporter 1 (URAT 1), organic anion transporter (OAT)1 or OAT3, and organic cation transporter (OCT)3, respectively. Indican 16-31 solute carrier family 22 member 3 Homo sapiens 206-211 26166660-0 2015 Apigenin inhibits indoxyl sulfate-induced endoplasmic reticulum stress and anti-proliferative pathways, CHOP and IL-6/p21, in human renal proximal tubular cells. Indican 18-33 DNA damage inducible transcript 3 Homo sapiens 104-108 26093151-8 2015 CB1R, collagen I, transforming growth factor (TGF)-beta, and alpha-smooth muscle actin (SMA) expression showed time- and dose-dependent upregulation in H9c2 cells treated with IS. Indican 176-178 cannabinoid receptor 1 (brain) Mus musculus 0-4 26093151-8 2015 CB1R, collagen I, transforming growth factor (TGF)-beta, and alpha-smooth muscle actin (SMA) expression showed time- and dose-dependent upregulation in H9c2 cells treated with IS. Indican 176-178 actin gamma 2, smooth muscle Rattus norvegicus 61-86 26093151-8 2015 CB1R, collagen I, transforming growth factor (TGF)-beta, and alpha-smooth muscle actin (SMA) expression showed time- and dose-dependent upregulation in H9c2 cells treated with IS. Indican 176-178 actin gamma 2, smooth muscle Rattus norvegicus 88-91 26230133-3 2015 The purple color is formed by a combination of indigo and indirubin produced as a result of phosphatase and sulfatase enzymatic activity of bacteria on indoxyl sulfate, under alkaline pH of the urine. Indican 152-167 arylsulfatase family member H Homo sapiens 108-117 26166660-11 2015 CONCLUSIONS: These results suggest that apigenin may inhibit IS-induced ER stress and expression of IL-6 and p21 proteins in HK-2 cells. Indican 61-63 interleukin 6 Homo sapiens 100-104 26166660-0 2015 Apigenin inhibits indoxyl sulfate-induced endoplasmic reticulum stress and anti-proliferative pathways, CHOP and IL-6/p21, in human renal proximal tubular cells. Indican 18-33 interleukin 6 Homo sapiens 113-117 26166660-11 2015 CONCLUSIONS: These results suggest that apigenin may inhibit IS-induced ER stress and expression of IL-6 and p21 proteins in HK-2 cells. Indican 61-63 H3 histone pseudogene 16 Homo sapiens 109-112 26166660-0 2015 Apigenin inhibits indoxyl sulfate-induced endoplasmic reticulum stress and anti-proliferative pathways, CHOP and IL-6/p21, in human renal proximal tubular cells. Indican 18-33 H3 histone pseudogene 16 Homo sapiens 118-121 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 11-26 mitogen-activated protein kinase 1 Homo sapiens 167-170 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 11-26 interleukin 6 Homo sapiens 171-175 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 11-26 H3 histone pseudogene 16 Homo sapiens 176-179 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 28-30 mitogen-activated protein kinase 1 Homo sapiens 167-170 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 28-30 interleukin 6 Homo sapiens 171-175 26166660-1 2015 OBJECTIVE: Indoxyl sulfate (IS) has been reported to induce endoplasmic reticulum (ER) stress in tubular cells and to inhibit the cell proliferation via ER stress and ERK/IL-6/p21 pathways. Indican 28-30 H3 histone pseudogene 16 Homo sapiens 176-179 25482161-6 2015 Endothelial cells were exposed to RGZ (5 and 10 mumol/L) and then treated with indoxyl sulphate (100 and 1000 mumol/L) for 48 h. Indoxyl sulphate upregulated intracellular cell adhesion molecule-1, vascular cell adhesion molecule-1 and monocyte chemotactic protein-1 expression. Indican 129-145 vascular cell adhesion molecule 1 Homo sapiens 198-266 25703824-0 2015 Indoxyl sulfate induces oxidative stress and hypertrophy in cardiomyocytes by inhibiting the AMPK/UCP2 signaling pathway. Indican 0-15 uncoupling protein 2 Rattus norvegicus 98-102 25703824-3 2015 In the present study, we aimed to determine whether UCP2 was involved in indoxyl sulfate-induced cardiomyocytes hypertrophy. Indican 73-88 uncoupling protein 2 Rattus norvegicus 52-56 25703824-6 2015 In contrast, cardiomyocytes transfected with the lentiviral vector carrying UCP2 gene were resistant to indoxyl sulfate-induced ROS production and cell hypertrophy. Indican 104-119 uncoupling protein 2 Rattus norvegicus 76-80 25703824-7 2015 Additionally, indoxyl sulfate-induced UCP2 reduction was correlated with the inhibition of AMP-activated protein kinase (AMPK) activity, while pretreatment with AICAR, an AMPK activator, effectively attenuated indoxyl sulfate-induced UCP2 down-regulation and hypertrophy in cardiomyocytes. Indican 14-29 uncoupling protein 2 Rattus norvegicus 38-42 25703824-7 2015 Additionally, indoxyl sulfate-induced UCP2 reduction was correlated with the inhibition of AMP-activated protein kinase (AMPK) activity, while pretreatment with AICAR, an AMPK activator, effectively attenuated indoxyl sulfate-induced UCP2 down-regulation and hypertrophy in cardiomyocytes. Indican 14-29 uncoupling protein 2 Rattus norvegicus 234-238 25703824-8 2015 Taken together, these results suggest that indoxyl sulfate-induced cardiomyocytes hypertrophy was partly due to the inhibition of AMPK/UCP2 signaling and the enhancement of oxidative stress. Indican 43-58 uncoupling protein 2 Rattus norvegicus 135-139 25482161-7 2015 Indoxyl sulphate also increased the abundance of NADPH oxidase 4 (NOX4) and nuclear factor (NF)-kappaB. Indican 0-16 NADPH oxidase 4 Homo sapiens 49-64 25482161-7 2015 Indoxyl sulphate also increased the abundance of NADPH oxidase 4 (NOX4) and nuclear factor (NF)-kappaB. Indican 0-16 NADPH oxidase 4 Homo sapiens 66-70 25482161-7 2015 Indoxyl sulphate also increased the abundance of NADPH oxidase 4 (NOX4) and nuclear factor (NF)-kappaB. Indican 0-16 nuclear factor kappa B subunit 1 Homo sapiens 76-102 25482161-8 2015 Both extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) signalling pathways were activated after 48 h treatment with indoxyl sulphate. Indican 162-178 mitogen-activated protein kinase 3 Homo sapiens 5-52 25482161-8 2015 Both extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) signalling pathways were activated after 48 h treatment with indoxyl sulphate. Indican 162-178 mitogen-activated protein kinase 14 Homo sapiens 57-93 25482161-8 2015 Both extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogen-activated protein kinase (MAPK) signalling pathways were activated after 48 h treatment with indoxyl sulphate. Indican 162-178 mitogen-activated protein kinase 3 Homo sapiens 95-99 25343458-0 2014 Indoxyl sulfate-induced activation of (pro)renin receptor promotes cell proliferation and tissue factor expression in vascular smooth muscle cells. Indican 0-15 renin Rattus norvegicus 43-48 25556305-2 2015 The present study aimed to determine whether nuclear factor-kappaB (NF-kappaB) p65, signal transducer and activator of transcription 3 (Stat3), and reactive oxygen species are involved in indoxyl sulfate-induced prorenin expression in cultured human proximal tubular cells (HK-2 cells). Indican 188-203 nuclear factor kappa B subunit 1 Homo sapiens 45-66 25556305-2 2015 The present study aimed to determine whether nuclear factor-kappaB (NF-kappaB) p65, signal transducer and activator of transcription 3 (Stat3), and reactive oxygen species are involved in indoxyl sulfate-induced prorenin expression in cultured human proximal tubular cells (HK-2 cells). Indican 188-203 nuclear factor kappa B subunit 1 Homo sapiens 68-77 25556305-2 2015 The present study aimed to determine whether nuclear factor-kappaB (NF-kappaB) p65, signal transducer and activator of transcription 3 (Stat3), and reactive oxygen species are involved in indoxyl sulfate-induced prorenin expression in cultured human proximal tubular cells (HK-2 cells). Indican 188-203 RELA proto-oncogene, NF-kB subunit Homo sapiens 79-82 25556305-2 2015 The present study aimed to determine whether nuclear factor-kappaB (NF-kappaB) p65, signal transducer and activator of transcription 3 (Stat3), and reactive oxygen species are involved in indoxyl sulfate-induced prorenin expression in cultured human proximal tubular cells (HK-2 cells). Indican 188-203 signal transducer and activator of transcription 3 Homo sapiens 84-134 25556305-2 2015 The present study aimed to determine whether nuclear factor-kappaB (NF-kappaB) p65, signal transducer and activator of transcription 3 (Stat3), and reactive oxygen species are involved in indoxyl sulfate-induced prorenin expression in cultured human proximal tubular cells (HK-2 cells). Indican 188-203 signal transducer and activator of transcription 3 Homo sapiens 136-141 25556305-5 2015 siRNAs specific to NF-kappaB p65 and Stat3 inhibited indoxyl sulfate-induced prorenin expression. Indican 53-68 nuclear factor kappa B subunit 1 Homo sapiens 19-28 25556305-5 2015 siRNAs specific to NF-kappaB p65 and Stat3 inhibited indoxyl sulfate-induced prorenin expression. Indican 53-68 RELA proto-oncogene, NF-kB subunit Homo sapiens 29-32 25556305-5 2015 siRNAs specific to NF-kappaB p65 and Stat3 inhibited indoxyl sulfate-induced prorenin expression. Indican 53-68 signal transducer and activator of transcription 3 Homo sapiens 37-42 25556305-7 2015 Indoxyl sulfate upregulates the expression of prorenin via NF-kappaB p65, Stat3, and reactive oxygen species in proximal tubular cells. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 59-68 25556305-7 2015 Indoxyl sulfate upregulates the expression of prorenin via NF-kappaB p65, Stat3, and reactive oxygen species in proximal tubular cells. Indican 0-15 RELA proto-oncogene, NF-kB subunit Homo sapiens 69-72 25556305-7 2015 Indoxyl sulfate upregulates the expression of prorenin via NF-kappaB p65, Stat3, and reactive oxygen species in proximal tubular cells. Indican 0-15 signal transducer and activator of transcription 3 Homo sapiens 74-79 25556305-0 2015 Indoxyl sulfate upregulates prorenin expression via nuclear factor-kappaB p65, signal transducer and activator of transcription 3, and reactive oxygen species in proximal tubular cells. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 52-73 25556305-0 2015 Indoxyl sulfate upregulates prorenin expression via nuclear factor-kappaB p65, signal transducer and activator of transcription 3, and reactive oxygen species in proximal tubular cells. Indican 0-15 RELA proto-oncogene, NF-kB subunit Homo sapiens 74-77 25556305-0 2015 Indoxyl sulfate upregulates prorenin expression via nuclear factor-kappaB p65, signal transducer and activator of transcription 3, and reactive oxygen species in proximal tubular cells. Indican 0-15 signal transducer and activator of transcription 3 Homo sapiens 79-129 25012179-5 2015 In cultured cells, indoxyl sulfate and p-cresol sulfate activated the EGF receptor and downstream signaling by enhancing receptor dimerization, and increased expression of matrix metalloproteinases 2 and 9 in an EGF receptor-dependent manner. Indican 19-34 matrix metallopeptidase 2 Mus musculus 172-205 25012179-6 2015 Treatment of mice with indoxyl sulfate or p-cresol sulfate significantly activated the renal EGF receptor and increased the tubulointerstitial expression of matrix metalloproteinases 2 and 9. Indican 23-38 matrix metallopeptidase 2 Mus musculus 157-190 25515305-7 2015 KEY FINDINGS: Indoxyl sulfate (IS) treatment alone resulted in ~ 3-fold increase in BCRP mRNA in Caco-2 cells. Indican 14-29 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 84-88 25515305-7 2015 KEY FINDINGS: Indoxyl sulfate (IS) treatment alone resulted in ~ 3-fold increase in BCRP mRNA in Caco-2 cells. Indican 31-33 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 84-88 25515305-8 2015 Membrane protein expression of BCRP in Caco-2 cells also was increased by 1.8-fold after treatment with IS. Indican 104-106 ATP binding cassette subfamily G member 2 (Junior blood group) Homo sapiens 31-35 24714415-1 2014 BACKGROUND: Indoxyl sulfate (IS) suppresses erythropoietin (EPO) activity and exerts renal damage. Indican 12-27 erythropoietin Homo sapiens 44-58 24812165-3 2014 Here, we performed a systematic review, selecting only studies in which, depending on the albumin concentration, real or extrapolated free concentrations of indoxyl sulfate and p-cresyl sulfate remained in the uremic range. Indican 157-172 albumin Homo sapiens 90-97 25244654-1 2014 Indoxyl sulfate is a uremic toxin and a ligand of the aryl-hydrocarbon receptor (AhR), a transcriptional regulator. Indican 0-15 aryl-hydrocarbon receptor Mus musculus 54-79 25244654-1 2014 Indoxyl sulfate is a uremic toxin and a ligand of the aryl-hydrocarbon receptor (AhR), a transcriptional regulator. Indican 0-15 aryl-hydrocarbon receptor Mus musculus 81-84 25244654-7 2014 In mice exposed to indoxyl sulfate for 2 h, isolated glomeruli manifested increased Cyp1a1 expression, indicating AhR activation. Indican 19-34 cytochrome P450, family 1, subfamily a, polypeptide 1 Mus musculus 84-90 25244654-7 2014 In mice exposed to indoxyl sulfate for 2 h, isolated glomeruli manifested increased Cyp1a1 expression, indicating AhR activation. Indican 19-34 aryl-hydrocarbon receptor Mus musculus 114-117 25244654-8 2014 After 8 w of indoxyl sulfate, podocytes showed foot process effacement, cytoplasmic vacuoles, and a focal granular and wrinkled pattern of podocin and synaptopodin expression. Indican 13-28 nephrosis 2, podocin Mus musculus 139-146 25244654-8 2014 After 8 w of indoxyl sulfate, podocytes showed foot process effacement, cytoplasmic vacuoles, and a focal granular and wrinkled pattern of podocin and synaptopodin expression. Indican 13-28 synaptopodin Mus musculus 151-163 25244654-9 2014 Furthermore, vimentin and AhR expression in the glomerulus was increased in the indoxyl sulfate-exposed glomeruli compared to controls. Indican 80-95 vimentin Mus musculus 13-21 25244654-9 2014 Furthermore, vimentin and AhR expression in the glomerulus was increased in the indoxyl sulfate-exposed glomeruli compared to controls. Indican 80-95 aryl-hydrocarbon receptor Mus musculus 26-29 25244654-11 2014 In vitro, immortalized-mouse podocytes exhibited AhR nuclear translocation beginning 30 min after 1 mM indoxyl sulfate exposure, and there was increased phospho-Rac1/Cdc42 at 2 h. After exposure to indoxyl sulfate for 24 h, mouse podocytes exhibited a pro-inflammatory phenotype, perturbed actin cytoskeleton, decreased expression of podocyte-specific genes, and decreased cell viability. Indican 198-213 aryl-hydrocarbon receptor Mus musculus 49-52 25244654-11 2014 In vitro, immortalized-mouse podocytes exhibited AhR nuclear translocation beginning 30 min after 1 mM indoxyl sulfate exposure, and there was increased phospho-Rac1/Cdc42 at 2 h. After exposure to indoxyl sulfate for 24 h, mouse podocytes exhibited a pro-inflammatory phenotype, perturbed actin cytoskeleton, decreased expression of podocyte-specific genes, and decreased cell viability. Indican 198-213 Rac family small GTPase 1 Mus musculus 161-165 25244654-11 2014 In vitro, immortalized-mouse podocytes exhibited AhR nuclear translocation beginning 30 min after 1 mM indoxyl sulfate exposure, and there was increased phospho-Rac1/Cdc42 at 2 h. After exposure to indoxyl sulfate for 24 h, mouse podocytes exhibited a pro-inflammatory phenotype, perturbed actin cytoskeleton, decreased expression of podocyte-specific genes, and decreased cell viability. Indican 198-213 cell division cycle 42 Mus musculus 166-171 25244654-13 2014 We propose that basal levels of AhR activity regulate podocyte function under normal conditions, and that increased activation of podocyte AhR by indoxyl sulfate contributes to progressive glomerular injury. Indican 146-161 aryl-hydrocarbon receptor Mus musculus 139-142 24714415-1 2014 BACKGROUND: Indoxyl sulfate (IS) suppresses erythropoietin (EPO) activity and exerts renal damage. Indican 12-27 erythropoietin Homo sapiens 60-63 24714415-1 2014 BACKGROUND: Indoxyl sulfate (IS) suppresses erythropoietin (EPO) activity and exerts renal damage. Indican 29-31 erythropoietin Homo sapiens 44-58 24714415-1 2014 BACKGROUND: Indoxyl sulfate (IS) suppresses erythropoietin (EPO) activity and exerts renal damage. Indican 29-31 erythropoietin Homo sapiens 60-63 25056788-0 2014 Indoxyl sulfate induces renin release and apoptosis of kidney mesangial cells. Indican 0-15 renin Rattus norvegicus 24-29 25011442-6 2014 RESULTS: Forty named and 34 unnamed metabolites were found to be associated with eGFR specified by the Chronic Kidney Disease Epidemiology Collaboration equation with creatine and 3-indoxyl sulfate showing the strongest positive (2.8 ml/min per 1.73 m(2) per +1 SD; 95% confidence interval, 2.1 to 3.5) and negative association (-14.2 ml/min per 1.73 m(2) per +1 SD; 95% confidence interval, -17.0 to -11.3), respectively. Indican 180-197 epidermal growth factor receptor Homo sapiens 81-85 25056788-8 2014 The mRNA expressions of pro-renin and ACE were upregulated in mesangial cells exposed to indoxyl sulfate. Indican 89-104 renin Rattus norvegicus 28-33 25056788-8 2014 The mRNA expressions of pro-renin and ACE were upregulated in mesangial cells exposed to indoxyl sulfate. Indican 89-104 angiotensin I converting enzyme Rattus norvegicus 38-41 25056788-9 2014 Level of renin and ACE was increased in response to indoxyl sulfate exposure in time-dependent fashion. Indican 52-67 renin Rattus norvegicus 9-14 25056788-9 2014 Level of renin and ACE was increased in response to indoxyl sulfate exposure in time-dependent fashion. Indican 52-67 angiotensin I converting enzyme Rattus norvegicus 19-22 24601883-0 2014 Indoxyl sulfate-induced activation of (pro)renin receptor is involved in expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 0-15 renin Rattus norvegicus 43-48 24051956-0 2014 Association of indoxyl sulfate with fibroblast growth factor 23 in patients with advanced chronic kidney disease. Indican 15-30 fibroblast growth factor 23 Homo sapiens 36-63 24601883-8 2014 N-acetylcysteine, an antioxidant, and diphenyleneiodonium, an inhibitor of nicotinamide adenine dinucleotide phosphate oxidase, suppressed indoxyl sulfate-induced PRR expression in proximal tubular cells. Indican 139-154 ATPase H+ transporting accessory protein 2 Homo sapiens 163-166 24601883-0 2014 Indoxyl sulfate-induced activation of (pro)renin receptor is involved in expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 87-96 24601883-9 2014 N-acetylcysteine prevented indoxyl sulfate-induced phosphorylation of Stat3 in proximal tubular cells. Indican 27-42 signal transducer and activator of transcription 3 Rattus norvegicus 70-75 24601883-10 2014 PRR small interfering RNA inhibited indoxyl sulfate-induced expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 36-51 ATPase H+ transporting accessory protein 2 Homo sapiens 0-3 24601883-0 2014 Indoxyl sulfate-induced activation of (pro)renin receptor is involved in expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 0-15 actin gamma 2, smooth muscle Rattus norvegicus 101-126 24601883-10 2014 PRR small interfering RNA inhibited indoxyl sulfate-induced expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 36-51 transforming growth factor, beta 1 Rattus norvegicus 74-83 24601883-2 2014 However, the role of indoxyl sulfate, a uremic toxin, in the activation of PRR is not clear. Indican 21-36 ATPase H+ transporting accessory protein 2 Homo sapiens 75-78 24601883-10 2014 PRR small interfering RNA inhibited indoxyl sulfate-induced expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 36-51 actin gamma 2, smooth muscle Rattus norvegicus 88-113 24601883-11 2014 Taken together, indoxyl sulfate-induced up-regulation of prorenin expression and activation of PRR through production of reactive oxygen species and activation of Stat3 and nuclear factor-kappaB play an important role in the expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 16-31 ATPase H+ transporting accessory protein 2 Homo sapiens 95-98 24601883-11 2014 Taken together, indoxyl sulfate-induced up-regulation of prorenin expression and activation of PRR through production of reactive oxygen species and activation of Stat3 and nuclear factor-kappaB play an important role in the expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 16-31 signal transducer and activator of transcription 3 Rattus norvegicus 163-168 24601883-11 2014 Taken together, indoxyl sulfate-induced up-regulation of prorenin expression and activation of PRR through production of reactive oxygen species and activation of Stat3 and nuclear factor-kappaB play an important role in the expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 16-31 transforming growth factor, beta 1 Rattus norvegicus 239-248 24601883-11 2014 Taken together, indoxyl sulfate-induced up-regulation of prorenin expression and activation of PRR through production of reactive oxygen species and activation of Stat3 and nuclear factor-kappaB play an important role in the expression of TGF-beta1 and alpha-smooth muscle actin in proximal tubular cells. Indican 16-31 actin gamma 2, smooth muscle Rattus norvegicus 253-278 24601883-12 2014 Thus, indoxyl sulfate-induced activation of prorenin/PRR might be involved in renal fibrosis. Indican 6-21 ATPase H+ transporting accessory protein 2 Homo sapiens 53-56 24601883-3 2014 The present study aimed to clarify the role of indoxyl sulfate in activation of PRR, in relation to renal expression of fibrotic genes. Indican 47-62 ATPase H+ transporting accessory protein 2 Homo sapiens 80-83 24601883-4 2014 Renal expression of PRR and renin/prorenin was up-regulated in chronic kidney disease rats compared with normal rats, whereas AST-120 suppressed these expression by reducing serum levels of indoxyl sulfate. Indican 190-205 ATPase H+ transporting accessory protein 2 Homo sapiens 20-23 24601883-5 2014 Furthermore, administration of indoxyl sulfate to normotensive and hypertensive rats increased renal expression of PRR and renin/prorenin. Indican 31-46 ATPase H+ transporting accessory protein 2 Homo sapiens 115-118 24601883-5 2014 Furthermore, administration of indoxyl sulfate to normotensive and hypertensive rats increased renal expression of PRR and renin/prorenin. Indican 31-46 renin Rattus norvegicus 123-128 24601883-6 2014 Indoxyl sulfate induced expression of PRR and prorenin in cultured human proximal tubular cells (HK-2 cells). Indican 0-15 ATPase H+ transporting accessory protein 2 Homo sapiens 38-41 24601883-7 2014 Indoxyl sulfate-induced PRR expression was inhibited by small interfering RNAs of signal transducer and activator of transcription 3 (Stat3) and nuclear factor-kappaB p65 in proximal tubular cells. Indican 0-15 ATPase H+ transporting accessory protein 2 Homo sapiens 24-27 24601883-7 2014 Indoxyl sulfate-induced PRR expression was inhibited by small interfering RNAs of signal transducer and activator of transcription 3 (Stat3) and nuclear factor-kappaB p65 in proximal tubular cells. Indican 0-15 signal transducer and activator of transcription 3 Rattus norvegicus 82-132 24601883-7 2014 Indoxyl sulfate-induced PRR expression was inhibited by small interfering RNAs of signal transducer and activator of transcription 3 (Stat3) and nuclear factor-kappaB p65 in proximal tubular cells. Indican 0-15 signal transducer and activator of transcription 3 Rattus norvegicus 134-139 24601883-7 2014 Indoxyl sulfate-induced PRR expression was inhibited by small interfering RNAs of signal transducer and activator of transcription 3 (Stat3) and nuclear factor-kappaB p65 in proximal tubular cells. Indican 0-15 synaptotagmin 1 Rattus norvegicus 167-170 24755682-0 2014 DPP-4 inhibitor attenuates toxic effects of indoxyl sulfate on kidney tubular cells. Indican 44-59 dipeptidyl peptidase 4 Homo sapiens 0-5 24614509-0 2014 Indoxyl sulfate downregulates expression of Mas receptor via OAT3/AhR/Stat3 pathway in proximal tubular cells. Indican 0-15 solute carrier family 22 member 8 Rattus norvegicus 61-65 24614509-0 2014 Indoxyl sulfate downregulates expression of Mas receptor via OAT3/AhR/Stat3 pathway in proximal tubular cells. Indican 0-15 aryl hydrocarbon receptor Rattus norvegicus 66-69 24614509-0 2014 Indoxyl sulfate downregulates expression of Mas receptor via OAT3/AhR/Stat3 pathway in proximal tubular cells. Indican 0-15 signal transducer and activator of transcription 3 Rattus norvegicus 70-75 24576840-5 2014 RESULTS: AST-120 significantly decreased both the total and free forms of indoxyl sulfate and p-cresol sulfate ranging from 21.9 to 58.3%. Indican 74-89 solute carrier family 17 member 5 Homo sapiens 9-12 24576840-7 2014 A significant association between the decrease of indoxyl sulfate and changes of sTWEAK and interleukin-6 was noted. Indican 50-65 interleukin 6 Homo sapiens 92-105 24576840-8 2014 CONCLUSIONS: AST-120 effectively decreased indoxyl sulfate and p-cresol sulfate levels in both total and free forms. Indican 43-58 solute carrier family 17 member 5 Homo sapiens 13-16 25579430-9 2014 Four uremic toxins, kynurenic acid, indole-3-acetic acid, indoxyl sulfate, and p-cresol, inhibited OATP1B1- and OATP1B3-mediated transport in a concentration-dependent manner, with IC50 values of 180, 770, 2700, and 4600 microM, respectively, for OATP1B1 and 180, 1100, 1300, and 1700 microM, respectively, for OATP1B3. Indican 58-73 solute carrier organic anion transporter family member 1B1 Homo sapiens 99-106 24727683-0 2014 Aryl hydrocarbon receptor mediates indoxyl sulfate-induced cellular senescence in human umbilical vein endothelial cells. Indican 35-50 aryl hydrocarbon receptor Homo sapiens 0-25 24727683-2 2014 We recently reported that indoxyl sulfate (IS), a uremic toxin, directly activates aryl hydrocarbon receptor (AhR) and generates oxidative stress through NADPH oxidase-4 in human umbilical vein endothelial cells (HUVECs). Indican 26-41 aryl hydrocarbon receptor Homo sapiens 83-108 24727683-2 2014 We recently reported that indoxyl sulfate (IS), a uremic toxin, directly activates aryl hydrocarbon receptor (AhR) and generates oxidative stress through NADPH oxidase-4 in human umbilical vein endothelial cells (HUVECs). Indican 26-41 aryl hydrocarbon receptor Homo sapiens 110-113 24727683-2 2014 We recently reported that indoxyl sulfate (IS), a uremic toxin, directly activates aryl hydrocarbon receptor (AhR) and generates oxidative stress through NADPH oxidase-4 in human umbilical vein endothelial cells (HUVECs). Indican 26-41 NADPH oxidase 4 Homo sapiens 154-169 24727683-9 2014 On the other hand, the AhR antagonists restored the IS-induced decrease in the NAD(+) content in association with an improvement in the iNampt activity and ameliorated the senescence-related changes. Indican 52-54 aryl hydrocarbon receptor Homo sapiens 23-26 25579430-9 2014 Four uremic toxins, kynurenic acid, indole-3-acetic acid, indoxyl sulfate, and p-cresol, inhibited OATP1B1- and OATP1B3-mediated transport in a concentration-dependent manner, with IC50 values of 180, 770, 2700, and 4600 microM, respectively, for OATP1B1 and 180, 1100, 1300, and 1700 microM, respectively, for OATP1B3. Indican 58-73 solute carrier organic anion transporter family member 1B3 Homo sapiens 112-119 25579430-9 2014 Four uremic toxins, kynurenic acid, indole-3-acetic acid, indoxyl sulfate, and p-cresol, inhibited OATP1B1- and OATP1B3-mediated transport in a concentration-dependent manner, with IC50 values of 180, 770, 2700, and 4600 microM, respectively, for OATP1B1 and 180, 1100, 1300, and 1700 microM, respectively, for OATP1B3. Indican 58-73 solute carrier organic anion transporter family member 1B1 Homo sapiens 247-254 25579430-9 2014 Four uremic toxins, kynurenic acid, indole-3-acetic acid, indoxyl sulfate, and p-cresol, inhibited OATP1B1- and OATP1B3-mediated transport in a concentration-dependent manner, with IC50 values of 180, 770, 2700, and 4600 microM, respectively, for OATP1B1 and 180, 1100, 1300, and 1700 microM, respectively, for OATP1B3. Indican 58-73 solute carrier organic anion transporter family member 1B3 Homo sapiens 311-318 25579430-12 2014 Moreover, OATP1B3 was involved in the transport of indoxyl sulfate. Indican 51-66 solute carrier organic anion transporter family member 1B3 Homo sapiens 10-17 24289746-11 2013 The expression of OAT, which is known to mediate the cellular uptake of IS, was detected in in the MC3T3-E1 cell line. Indican 72-74 ornithine aminotransferase Mus musculus 18-21 25376195-0 2014 Indoxyl sulfate induces IL-6 expression in vascular endothelial and smooth muscle cells through OAT3-mediated uptake and activation of AhR/NF-kappaB pathway. Indican 0-15 interleukin 6 Homo sapiens 24-28 25376195-0 2014 Indoxyl sulfate induces IL-6 expression in vascular endothelial and smooth muscle cells through OAT3-mediated uptake and activation of AhR/NF-kappaB pathway. Indican 0-15 solute carrier family 22 member 8 Homo sapiens 96-100 25376195-0 2014 Indoxyl sulfate induces IL-6 expression in vascular endothelial and smooth muscle cells through OAT3-mediated uptake and activation of AhR/NF-kappaB pathway. Indican 0-15 aryl hydrocarbon receptor Homo sapiens 135-138 25376195-2 2014 The present study aimed to determine the effects of indoxyl sulfate (IS) on IL-6 expression in vascular cells. Indican 52-67 interleukin 6 Homo sapiens 76-80 25376195-2 2014 The present study aimed to determine the effects of indoxyl sulfate (IS) on IL-6 expression in vascular cells. Indican 69-71 interleukin 6 Homo sapiens 76-80 25376195-12 2014 Thus, AhR is responsible for IS-induced p65 signaling transduction. Indican 29-31 aryl hydrocarbon receptor Homo sapiens 6-9 25376195-12 2014 Thus, AhR is responsible for IS-induced p65 signaling transduction. Indican 29-31 RELA proto-oncogene, NF-kB subunit Homo sapiens 40-43 23636172-5 2013 We found an increase in endothelial expression of tissue factor in response to indoxyl sulfate and IAA and upregulation of eight genes regulated by the transcription factor aryl hydrocarbon receptor (AHR). Indican 79-94 coagulation factor III, tissue factor Homo sapiens 50-63 24188099-6 2013 RESULTS: A 48 hours exposure to indoxyl sulfate significantly increased [Ca(2+)]i (>= 300 muM), significantly decreased forward scatter (>= 300 muM) and significantly increased annexin-V-binding (>= 50 muM). Indican 32-47 annexin A5 Homo sapiens 183-192 24188099-7 2013 Indoxyl sulfate (150 muM) induced annexin-V-binding was virtually abolished in the nominal absence of extracellular Ca(2+). Indican 0-15 annexin A5 Homo sapiens 34-43 23792300-0 2013 Indoxyl sulfate signals for rapid mRNA stabilization of Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2) and suppresses the expression of hypoxia-inducible genes in experimental CKD and uremia. Indican 0-15 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 Homo sapiens 56-135 23792300-0 2013 Indoxyl sulfate signals for rapid mRNA stabilization of Cbp/p300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 2 (CITED2) and suppresses the expression of hypoxia-inducible genes in experimental CKD and uremia. Indican 0-15 Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 2 Homo sapiens 137-143 23636172-10 2013 Circulating tissue factor levels were positively correlated with plasma indoxyl sulfate and IAA. Indican 72-87 coagulation factor III, tissue factor Homo sapiens 12-25 23874392-0 2013 Indoxyl sulfate down-regulates SLCO4C1 transporter through up-regulation of GATA3. Indican 0-15 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 31-38 23813557-9 2013 A linear relationship was observed between estimated GFR and clearances of p-cresyl sulfate (R(2)=0.50, P<0.001) and indoxyl sulfate (R(2)=0.55, P<0.001). Indican 120-135 Rap guanine nucleotide exchange factor 5 Homo sapiens 53-56 23813557-11 2013 Indoxyl sulfate concentrations were associated (R(2)=0.74) with estimated GFR, generation rate (both P<0.001), age (P<0.05), and sex (P<0.05). Indican 0-15 Rap guanine nucleotide exchange factor 5 Homo sapiens 74-77 23813557-12 2013 CONCLUSIONS: Estimated GFR provides an acceptable estimate of renal clearance of p-cresyl sulfate and indoxyl sulfate. Indican 102-117 Rap guanine nucleotide exchange factor 5 Homo sapiens 23-26 23707770-1 2013 We investigated the effects of JBP485 (an anti-inflammatory dipeptide and a substrate of OAT) on regulation of the expression and function of renal Oat1 and Oat3, which can accelerate the excretion of accumulated uremic toxins (e.g. indoxyl sulfate) in the kidney to improve gentamicin-induced ARF in rats. Indican 233-248 solute carrier family 22 member 6 Rattus norvegicus 148-152 23874392-0 2013 Indoxyl sulfate down-regulates SLCO4C1 transporter through up-regulation of GATA3. Indican 0-15 GATA binding protein 3 Rattus norvegicus 76-81 23874392-3 2013 Here we report that indoxyl sulfate, one of the potent uremic toxins, directly suppresses the renal-specific organic anion transporter SLCO4C1 expression through a transcription factor GATA3. Indican 20-35 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 135-142 23874392-3 2013 Here we report that indoxyl sulfate, one of the potent uremic toxins, directly suppresses the renal-specific organic anion transporter SLCO4C1 expression through a transcription factor GATA3. Indican 20-35 GATA binding protein 3 Rattus norvegicus 185-190 23874392-4 2013 The promoter region of SLCO4C1 gene has several GATA motifs, and indoxyl sulfate up-regulated GATA3 mRNA and subsequently down-regulated SLCO4C1 mRNA. Indican 65-80 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 23-30 23874392-4 2013 The promoter region of SLCO4C1 gene has several GATA motifs, and indoxyl sulfate up-regulated GATA3 mRNA and subsequently down-regulated SLCO4C1 mRNA. Indican 65-80 GATA binding protein 3 Rattus norvegicus 94-99 23874392-4 2013 The promoter region of SLCO4C1 gene has several GATA motifs, and indoxyl sulfate up-regulated GATA3 mRNA and subsequently down-regulated SLCO4C1 mRNA. Indican 65-80 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 137-144 23874392-6 2013 Administration of indoxyl sulfate in rats reduced renal expression of slco4c1 and under this condition, plasma level of guanidinosuccinate, one of the preferable substrates of slco4c1, was significantly increased without changing plasma creatinine. Indican 18-33 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 70-77 23874392-6 2013 Administration of indoxyl sulfate in rats reduced renal expression of slco4c1 and under this condition, plasma level of guanidinosuccinate, one of the preferable substrates of slco4c1, was significantly increased without changing plasma creatinine. Indican 18-33 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 176-183 23874392-8 2013 These data suggest that the removal of indoxyl sulfate and blocking its signal pathway may help to restore the SLCO4C1-mediated renal excretion of uremic toxins in CKD. Indican 39-54 solute carrier organic anion transporter family, member 4C1 Rattus norvegicus 111-118 23362306-0 2013 Reduction of indoxyl sulfate by AST-120 attenuates monocyte inflammation related to chronic kidney disease. Indican 13-28 solute carrier family 17 member 5 Homo sapiens 32-35 23407882-0 2013 CREB, NF-kappaB, and NADPH oxidase coordinately upregulate indoxyl sulfate-induced angiotensinogen expression in proximal tubular cells. Indican 59-74 cAMP responsive element binding protein 1 Homo sapiens 0-4 23407882-0 2013 CREB, NF-kappaB, and NADPH oxidase coordinately upregulate indoxyl sulfate-induced angiotensinogen expression in proximal tubular cells. Indican 59-74 nuclear factor kappa B subunit 1 Homo sapiens 6-15 23407882-3 2013 Indoxyl sulfate induced expression of AGT in rat renal cortex and in cultured human proximal tubular cells (HK-2). Indican 0-15 angiotensinogen Rattus norvegicus 38-41 23407882-7 2013 Both NAC and DPI suppressed indoxyl sulfate-induced expression of NF-kappaB p65 and CREB. Indican 28-43 nuclear factor kappa B subunit 1 Homo sapiens 66-75 23407882-0 2013 CREB, NF-kappaB, and NADPH oxidase coordinately upregulate indoxyl sulfate-induced angiotensinogen expression in proximal tubular cells. Indican 59-74 angiotensinogen Homo sapiens 83-98 23407882-7 2013 Both NAC and DPI suppressed indoxyl sulfate-induced expression of NF-kappaB p65 and CREB. Indican 28-43 RELA proto-oncogene, NF-kB subunit Homo sapiens 76-79 23407882-2 2013 The present study aimed to determine the relationship between indoxyl sulfate and the upregulation of AGT expression in proximal tubular cells. Indican 62-77 angiotensinogen Homo sapiens 102-105 23407882-7 2013 Both NAC and DPI suppressed indoxyl sulfate-induced expression of NF-kappaB p65 and CREB. Indican 28-43 cAMP responsive element binding protein 1 Homo sapiens 84-88 23407882-11 2013 Taken together, CREB, NF-kappaB, and NOX4 coordinately upregulate indoxyl sulfate-induced AGT expression in proximal tubular cells. Indican 66-81 cAMP responsive element binding protein 1 Homo sapiens 16-20 23407882-11 2013 Taken together, CREB, NF-kappaB, and NOX4 coordinately upregulate indoxyl sulfate-induced AGT expression in proximal tubular cells. Indican 66-81 nuclear factor kappa B subunit 1 Homo sapiens 22-31 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 22-37 cAMP responsive element binding protein 1 Homo sapiens 0-4 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 27-42 cAMP responsive element binding protein 1 Homo sapiens 70-107 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 22-37 nuclear factor kappa B subunit 1 Homo sapiens 46-55 23407882-11 2013 Taken together, CREB, NF-kappaB, and NOX4 coordinately upregulate indoxyl sulfate-induced AGT expression in proximal tubular cells. Indican 66-81 NADPH oxidase 4 Homo sapiens 37-41 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 22-37 RELA proto-oncogene, NF-kB subunit Homo sapiens 56-59 23407882-11 2013 Taken together, CREB, NF-kappaB, and NOX4 coordinately upregulate indoxyl sulfate-induced AGT expression in proximal tubular cells. Indican 66-81 angiotensinogen Homo sapiens 90-93 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 27-42 cAMP responsive element binding protein 1 Homo sapiens 109-113 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 140-155 RELA proto-oncogene, NF-kB subunit Homo sapiens 56-59 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 27-42 cAMP responsive element binding protein 1 Homo sapiens 173-177 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 140-155 nuclear factor kappa B subunit 1 Homo sapiens 85-94 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 27-42 angiotensinogen Homo sapiens 212-215 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 140-155 nuclear factor kappa B subunit 1 Homo sapiens 85-94 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 188-203 cAMP responsive element binding protein 1 Homo sapiens 70-107 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 140-155 RELA proto-oncogene, NF-kB subunit Homo sapiens 120-123 23407882-8 2013 CREB siRNA suppressed indoxyl sulfate-induced NF-kappaB p65 expression, whereas both NF-kappaB inhibitors and NF-kappaB p65 siRNA prevented indoxyl sulfate-induced CREB expression. Indican 140-155 cAMP responsive element binding protein 1 Homo sapiens 164-168 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 188-203 cAMP responsive element binding protein 1 Homo sapiens 109-113 23407882-9 2013 Furthermore, we focused on the expression of NADPH oxidase 4 (NOX4), because indoxyl sulfate induced NOX4 expression in vascular smooth muscle cells and vascular endothelial cells. Indican 77-92 NADPH oxidase 4 Homo sapiens 45-60 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 188-203 cAMP responsive element binding protein 1 Homo sapiens 173-177 23407882-9 2013 Furthermore, we focused on the expression of NADPH oxidase 4 (NOX4), because indoxyl sulfate induced NOX4 expression in vascular smooth muscle cells and vascular endothelial cells. Indican 77-92 NADPH oxidase 4 Homo sapiens 62-66 23407882-4 2013 In proximal tubular cells, indoxyl sulfate induced phosphorylation of cAMP response element-binding protein (CREB) on Ser-133, and small interfering RNA (siRNA) specific to CREB inhibited indoxyl sulfate-induced AGT expression. Indican 188-203 angiotensinogen Homo sapiens 212-215 23407882-9 2013 Furthermore, we focused on the expression of NADPH oxidase 4 (NOX4), because indoxyl sulfate induced NOX4 expression in vascular smooth muscle cells and vascular endothelial cells. Indican 77-92 NADPH oxidase 4 Homo sapiens 101-105 23407882-10 2013 Indoxyl sulfate induced the expression of NOX4 in proximal tubular cells, which was suppressed by NAC, DPI, NF-kappaB inhibitors, NF-kappaB p65 siRNA, and CREB siRNA. Indican 0-15 NADPH oxidase 4 Homo sapiens 42-46 23407882-10 2013 Indoxyl sulfate induced the expression of NOX4 in proximal tubular cells, which was suppressed by NAC, DPI, NF-kappaB inhibitors, NF-kappaB p65 siRNA, and CREB siRNA. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 108-117 23407882-10 2013 Indoxyl sulfate induced the expression of NOX4 in proximal tubular cells, which was suppressed by NAC, DPI, NF-kappaB inhibitors, NF-kappaB p65 siRNA, and CREB siRNA. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 130-139 23407882-10 2013 Indoxyl sulfate induced the expression of NOX4 in proximal tubular cells, which was suppressed by NAC, DPI, NF-kappaB inhibitors, NF-kappaB p65 siRNA, and CREB siRNA. Indican 0-15 RELA proto-oncogene, NF-kB subunit Homo sapiens 140-143 23407882-10 2013 Indoxyl sulfate induced the expression of NOX4 in proximal tubular cells, which was suppressed by NAC, DPI, NF-kappaB inhibitors, NF-kappaB p65 siRNA, and CREB siRNA. Indican 0-15 cAMP responsive element binding protein 1 Homo sapiens 155-159 23407882-5 2013 Our previous study demonstrated that indoxyl sulfate activated nuclear factor-kappaB (NF-kappaB) through reactive oxygen species (ROS) production. Indican 37-52 nuclear factor kappa B subunit 1 Homo sapiens 86-95 23265586-6 2013 Indoxyl sulfate (IS) is a uremic retention solute proven with pro-proliferative effect on rat VSMCs, and we further studied the expression of GLUT1 in rat A7r5 rat embryonic aortic cells stimulated by IS in the presence or absence of phloretin, a GLUT1 inhibitor, to explore the pathogenic role of GLUT1 in uremic vasculopathy. Indican 0-15 solute carrier family 2 member 1 Rattus norvegicus 142-147 23496811-0 2013 Indoxyl sulfate, a uremic toxin, downregulates renal expression of Nrf2 through activation of NF-kappaB. Indican 0-15 NFE2 like bZIP transcription factor 2 Rattus norvegicus 67-71 23496811-4 2013 The present study aimed to determine whether indoxyl sulfate downregulates Nrf2 expression in human proximal tubular cells and rat kidneys and whether AST-120 upregulates Nrf2 expression in CKD rat kidneys. Indican 45-60 NFE2 like bZIP transcription factor 2 Homo sapiens 75-79 23496811-5 2013 METHODS: Effects of indoxyl sulfate on expression of Nrf2 were determined using HK-2 cells as human proximal tubular cells and the following animals: (1) Dahl salt-resistant normotensive rats (DN), (2) Dahl salt-resistant normotensive indoxyl sulfate-administered rats (DN+IS), (3) Dahl salt-sensitive hypertensive rats (DH), and (4) Dahl salt-sensitive hypertensive indoxyl sulfate-administered rats (DH+IS). Indican 20-35 NFE2 like bZIP transcription factor 2 Homo sapiens 53-57 23201429-0 2013 Indoxyl sulfate upregulates renal expression of ICAM-1 via production of ROS and activation of NF-kappaB and p53 in proximal tubular cells. Indican 0-15 intercellular adhesion molecule 1 Rattus norvegicus 48-54 23201429-0 2013 Indoxyl sulfate upregulates renal expression of ICAM-1 via production of ROS and activation of NF-kappaB and p53 in proximal tubular cells. Indican 0-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 109-112 23201429-2 2013 The present study aimed to determine if indoxyl sulfate, a uremic toxin, regulates renal expression of ICAM-1. Indican 40-55 intercellular adhesion molecule 1 Rattus norvegicus 103-109 23201429-3 2013 MAIN METHODS: The effect of indoxyl sulfate on expression of ICAM-1 was determined using human proximal tubular cells (HK-2 cells) and the following animals: (1) Dahl salt-resistant normotensive rats (DN), (2) Dahl salt-resistant normotensive indoxyl sulfate-administered rats (DN+IS), (3) Dahl salt-sensitive hypertensive rats (DH), and (4) Dahl salt-sensitive hypertensive indoxyl sulfate-administered rats (DH+IS). Indican 28-43 intercellular adhesion molecule 1 Homo sapiens 61-67 23496811-7 2013 RESULTS: Indoxyl sulfate downregulated Nrf2 expression in HK-2 cells. Indican 9-24 NFE2 like bZIP transcription factor 2 Rattus norvegicus 39-43 23496811-8 2013 The indoxyl sulfate-induced downregulation of Nrf2 expression was alleviated by an inhibitor of nuclear factor-kappaB (NF-kappaB) (pyrrolidine dithiocarbamate) and small interfering RNA specific to NF-kappaB p65. Indican 4-19 NFE2 like bZIP transcription factor 2 Rattus norvegicus 46-50 23496811-10 2013 Thus, indoxyl sulfate, as well as hypertension, downregulated renal expression of Nrf2 in rats. Indican 6-21 NFE2 like bZIP transcription factor 2 Rattus norvegicus 82-86 23496811-12 2013 CONCLUSIONS: Indoxyl sulfate downregulates renal expression of Nrf2 through activation of NF-kappaB, followed by downregulation of HO-1 and NQO1 and increased production of ROS. Indican 13-28 NFE2 like bZIP transcription factor 2 Rattus norvegicus 63-67 23496811-12 2013 CONCLUSIONS: Indoxyl sulfate downregulates renal expression of Nrf2 through activation of NF-kappaB, followed by downregulation of HO-1 and NQO1 and increased production of ROS. Indican 13-28 heme oxygenase 1 Rattus norvegicus 131-135 23496811-12 2013 CONCLUSIONS: Indoxyl sulfate downregulates renal expression of Nrf2 through activation of NF-kappaB, followed by downregulation of HO-1 and NQO1 and increased production of ROS. Indican 13-28 NAD(P)H quinone dehydrogenase 1 Rattus norvegicus 140-144 23496811-13 2013 Further, AST-120 upregulates renal expression of Nrf2 in CKD rats by removing serum indoxyl sulfate, followed by upregulation of HO-1 and NQO1 and decreased production of ROS. Indican 84-99 NFE2 like bZIP transcription factor 2 Rattus norvegicus 49-53 23201429-7 2013 Indoxyl sulfate upregulated mRNA and protein expression of ICAM-1 in HK-2 cells. Indican 0-15 intercellular adhesion molecule 1 Rattus norvegicus 59-65 23201429-8 2013 Inhibitors of NADPH oxidase (diphenylene iodonium chloride), NF-kappaB (isohelenin) and p53 (pifithrin-alpha,p-nitro) suppressed indoxyl sulfate-induced expression of ICAM-1 mRNA and protein in HK-2 cells. Indican 129-144 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 88-91 23201429-8 2013 Inhibitors of NADPH oxidase (diphenylene iodonium chloride), NF-kappaB (isohelenin) and p53 (pifithrin-alpha,p-nitro) suppressed indoxyl sulfate-induced expression of ICAM-1 mRNA and protein in HK-2 cells. Indican 129-144 intercellular adhesion molecule 1 Rattus norvegicus 167-173 23201429-9 2013 SIGNIFICANCE: Indoxyl sulfate upregulated renal expression of ICAM-1 through production of reactive oxygen species (ROS) such as superoxide, and activation of NF-kappaB and p53 in proximal tubular cells. Indican 14-29 intercellular adhesion molecule 1 Rattus norvegicus 62-68 23201429-9 2013 SIGNIFICANCE: Indoxyl sulfate upregulated renal expression of ICAM-1 through production of reactive oxygen species (ROS) such as superoxide, and activation of NF-kappaB and p53 in proximal tubular cells. Indican 14-29 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 173-176 23201429-10 2013 Further, administration of indoxyl sulfate promoted ICAM-1 expression in rat kidneys. Indican 27-42 intercellular adhesion molecule 1 Rattus norvegicus 52-58 23201429-11 2013 Thus, accumulation of indoxyl sulfate in chronic kidney disease might be involved in the pathogenesis of tubulointerstitial injury through induction of ICAM-1 in the kidney. Indican 22-37 intercellular adhesion molecule 1 Rattus norvegicus 152-158 23227912-7 2013 Indoxyl sulfate and p-cresyl sulfate stimulate progressive tubulointerstitial fibrosis by increasing the expression of transforming growth factor-beta1 (TGF-beta1). Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 119-151 23227912-7 2013 Indoxyl sulfate and p-cresyl sulfate stimulate progressive tubulointerstitial fibrosis by increasing the expression of transforming growth factor-beta1 (TGF-beta1). Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 153-162 23265586-6 2013 Indoxyl sulfate (IS) is a uremic retention solute proven with pro-proliferative effect on rat VSMCs, and we further studied the expression of GLUT1 in rat A7r5 rat embryonic aortic cells stimulated by IS in the presence or absence of phloretin, a GLUT1 inhibitor, to explore the pathogenic role of GLUT1 in uremic vasculopathy. Indican 0-15 solute carrier family 2 member 1 Rattus norvegicus 247-252 23265586-6 2013 Indoxyl sulfate (IS) is a uremic retention solute proven with pro-proliferative effect on rat VSMCs, and we further studied the expression of GLUT1 in rat A7r5 rat embryonic aortic cells stimulated by IS in the presence or absence of phloretin, a GLUT1 inhibitor, to explore the pathogenic role of GLUT1 in uremic vasculopathy. Indican 0-15 solute carrier family 2 member 1 Rattus norvegicus 247-252 23269489-9 2013 We show further that TF undergoes ubiquitination at baseline and that uremic serum, indole-3-acetic acid, and indoxyl sulfate significantly prolong TF half-life by inhibiting its ubiquitination. Indican 110-125 coagulation factor III, tissue factor Homo sapiens 148-150 23363842-0 2013 Indoxyl sulfate enhances p53-TGF-beta1-Smad3 pathway in proximal tubular cells. Indican 0-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 25-28 23363842-0 2013 Indoxyl sulfate enhances p53-TGF-beta1-Smad3 pathway in proximal tubular cells. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 29-38 23363842-6 2013 Further, indoxyl sulfate stimulated TGF-beta1-induced expression of alpha-SMA by enhancing Smad3 expression and TGF-beta1-induced Smad3 phosphorylation. Indican 9-24 transforming growth factor, beta 1 Rattus norvegicus 36-45 23363842-0 2013 Indoxyl sulfate enhances p53-TGF-beta1-Smad3 pathway in proximal tubular cells. Indican 0-15 SMAD family member 3 Rattus norvegicus 39-44 23363842-6 2013 Further, indoxyl sulfate stimulated TGF-beta1-induced expression of alpha-SMA by enhancing Smad3 expression and TGF-beta1-induced Smad3 phosphorylation. Indican 9-24 actin gamma 2, smooth muscle Rattus norvegicus 68-77 23363842-6 2013 Further, indoxyl sulfate stimulated TGF-beta1-induced expression of alpha-SMA by enhancing Smad3 expression and TGF-beta1-induced Smad3 phosphorylation. Indican 9-24 SMAD family member 3 Rattus norvegicus 91-96 23363842-1 2013 BACKGROUND/AIM: Indoxyl sulfate-induced activation of nuclear factor (NF)-kB promotes transforming growth factor (TGF)-beta1 in human proximal tubular cells (HK-2 cells). Indican 16-31 transforming growth factor beta 1 Homo sapiens 86-124 23363842-6 2013 Further, indoxyl sulfate stimulated TGF-beta1-induced expression of alpha-SMA by enhancing Smad3 expression and TGF-beta1-induced Smad3 phosphorylation. Indican 9-24 transforming growth factor, beta 1 Rattus norvegicus 112-121 23363842-3 2013 METHODS: The effects of indoxyl sulfate on the expression of TGF-beta1, Smad3, and alpha-smooth muscle actin (alpha-SMA) were determined using HK-2 cells. Indican 24-39 transforming growth factor, beta 1 Rattus norvegicus 61-70 23363842-6 2013 Further, indoxyl sulfate stimulated TGF-beta1-induced expression of alpha-SMA by enhancing Smad3 expression and TGF-beta1-induced Smad3 phosphorylation. Indican 9-24 SMAD family member 3 Rattus norvegicus 130-135 23363842-7 2013 Indoxyl sulfate induced phosphorylation of extracellular signal-regulated kinase (ERK). Indican 0-15 Eph receptor B1 Rattus norvegicus 43-80 23363842-3 2013 METHODS: The effects of indoxyl sulfate on the expression of TGF-beta1, Smad3, and alpha-smooth muscle actin (alpha-SMA) were determined using HK-2 cells. Indican 24-39 SMAD family member 3 Rattus norvegicus 72-77 23363842-7 2013 Indoxyl sulfate induced phosphorylation of extracellular signal-regulated kinase (ERK). Indican 0-15 Eph receptor B1 Rattus norvegicus 82-85 23363842-3 2013 METHODS: The effects of indoxyl sulfate on the expression of TGF-beta1, Smad3, and alpha-smooth muscle actin (alpha-SMA) were determined using HK-2 cells. Indican 24-39 actin gamma 2, smooth muscle Rattus norvegicus 83-108 23363842-8 2013 U0126, an inhibitor of ERK pathway, prevented indoxyl sulfate-induced upregulation of Smad3 expression. Indican 46-61 Eph receptor B1 Rattus norvegicus 23-26 23363842-8 2013 U0126, an inhibitor of ERK pathway, prevented indoxyl sulfate-induced upregulation of Smad3 expression. Indican 46-61 SMAD family member 3 Rattus norvegicus 86-91 23363842-3 2013 METHODS: The effects of indoxyl sulfate on the expression of TGF-beta1, Smad3, and alpha-smooth muscle actin (alpha-SMA) were determined using HK-2 cells. Indican 24-39 actin gamma 2, smooth muscle Rattus norvegicus 110-119 23363842-9 2013 Immunohistochemistry demonstrated that TGF-beta1 and Smad3 were localized in renal tubular cells, and that indoxyl sulfate increased the TGF-beta1 and Smad3-positive area in the kidney. Indican 107-122 transforming growth factor, beta 1 Rattus norvegicus 137-146 23363842-9 2013 Immunohistochemistry demonstrated that TGF-beta1 and Smad3 were localized in renal tubular cells, and that indoxyl sulfate increased the TGF-beta1 and Smad3-positive area in the kidney. Indican 107-122 SMAD family member 3 Rattus norvegicus 151-156 23363842-10 2013 CONCLUSION: Indoxyl sulfate stimulates p53-induced TGF-beta1 expression and TGF-beta1-induced alpha-SMA expression in proximal tubular cells. Indican 12-27 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 39-42 23363842-5 2013 RESULTS: Both indoxyl sulfate and nutlin-3, a specific p53 inducer, stimulated TGF-beta1 expression, which was suppressed by pifithrin-alpha, p-nitro, a p53 inhibitor. Indican 14-29 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 55-58 23363842-10 2013 CONCLUSION: Indoxyl sulfate stimulates p53-induced TGF-beta1 expression and TGF-beta1-induced alpha-SMA expression in proximal tubular cells. Indican 12-27 transforming growth factor, beta 1 Rattus norvegicus 51-60 23363842-10 2013 CONCLUSION: Indoxyl sulfate stimulates p53-induced TGF-beta1 expression and TGF-beta1-induced alpha-SMA expression in proximal tubular cells. Indican 12-27 transforming growth factor, beta 1 Rattus norvegicus 76-85 23363842-11 2013 Indoxyl sulfate-induced Smad3 accelerates TGF-beta1-induced alpha-SMA expression through ERK activation. Indican 0-15 SMAD family member 3 Rattus norvegicus 24-29 23363842-5 2013 RESULTS: Both indoxyl sulfate and nutlin-3, a specific p53 inducer, stimulated TGF-beta1 expression, which was suppressed by pifithrin-alpha, p-nitro, a p53 inhibitor. Indican 14-29 transforming growth factor, beta 1 Rattus norvegicus 79-88 23363842-11 2013 Indoxyl sulfate-induced Smad3 accelerates TGF-beta1-induced alpha-SMA expression through ERK activation. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 42-51 23363842-11 2013 Indoxyl sulfate-induced Smad3 accelerates TGF-beta1-induced alpha-SMA expression through ERK activation. Indican 0-15 actin gamma 2, smooth muscle Rattus norvegicus 60-69 23363842-5 2013 RESULTS: Both indoxyl sulfate and nutlin-3, a specific p53 inducer, stimulated TGF-beta1 expression, which was suppressed by pifithrin-alpha, p-nitro, a p53 inhibitor. Indican 14-29 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 153-156 23363842-11 2013 Indoxyl sulfate-induced Smad3 accelerates TGF-beta1-induced alpha-SMA expression through ERK activation. Indican 0-15 Eph receptor B1 Rattus norvegicus 89-92 23363842-12 2013 Thus, indoxyl sulfate enhances p53-TGF-beta1-Smad3 pathway in proximal tubular cells. Indican 6-21 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 31-34 23363842-12 2013 Thus, indoxyl sulfate enhances p53-TGF-beta1-Smad3 pathway in proximal tubular cells. Indican 6-21 transforming growth factor, beta 1 Rattus norvegicus 35-44 23363842-12 2013 Thus, indoxyl sulfate enhances p53-TGF-beta1-Smad3 pathway in proximal tubular cells. Indican 6-21 SMAD family member 3 Rattus norvegicus 45-50 23017367-6 2013 Furthermore, a wide variety of uremic toxins, including indole-3-acetic acid, indoxyl sulfate, phenylacetic acid and kynurenic acid, reduced 7-OHC glucuronidation with more than 30% as compared with controls (p<0.05), whereas UGT1A and UGT2B protein expressions remained unaltered. Indican 78-93 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 229-234 23037589-0 2013 Activation of aryl hydrocarbon receptor mediates indoxyl sulfate-induced monocyte chemoattractant protein-1 expression in human umbilical vein endothelial cells. Indican 49-64 aryl hydrocarbon receptor Homo sapiens 14-39 23037589-0 2013 Activation of aryl hydrocarbon receptor mediates indoxyl sulfate-induced monocyte chemoattractant protein-1 expression in human umbilical vein endothelial cells. Indican 49-64 C-C motif chemokine ligand 2 Homo sapiens 73-107 22633673-0 2012 Antagonists of organic anion transporters 1 and 3 ameliorate adverse cardiac remodelling induced by uremic toxin indoxyl sulfate. Indican 113-128 solute carrier family 22 member 6 Homo sapiens 15-49 23085347-0 2012 Amelioration of uremic toxin indoxyl sulfate-induced endothelial cell dysfunction by Klotho protein. Indican 29-44 klotho Homo sapiens 85-91 23337206-0 2013 Indoxyl sulfate counteracts endothelial effects of erythropoietin through suppression of Akt phosphorylation. Indican 0-15 erythropoietin Homo sapiens 51-65 23337206-0 2013 Indoxyl sulfate counteracts endothelial effects of erythropoietin through suppression of Akt phosphorylation. Indican 0-15 AKT serine/threonine kinase 1 Homo sapiens 89-92 23337206-5 2013 The aim of the present study was to determine the effect of indoxyl sulfate on the extra-hematopoietic functions of EPO in human umbilical vein endothelial cells (HUVECs). Indican 60-75 erythropoietin Homo sapiens 116-119 23337206-7 2013 Indoxyl sulfate suppressed EPO-induced survival/proliferation, anti-apoptosis function, phosphorylation of endothelial nitric oxide synthase, and the expression of thrombospondin-1, an erythroid-stimulating factor, in HUVECs. Indican 0-15 erythropoietin Homo sapiens 27-30 23337206-7 2013 Indoxyl sulfate suppressed EPO-induced survival/proliferation, anti-apoptosis function, phosphorylation of endothelial nitric oxide synthase, and the expression of thrombospondin-1, an erythroid-stimulating factor, in HUVECs. Indican 0-15 thrombospondin 1 Homo sapiens 164-180 23337206-8 2013 Although EPO induced phosphorylation of both Akt and extracellular signal-regulated kinases (ERK) in HUVECs, indoxyl sulfate suppressed phosphorylation of Akt but not ERK. Indican 109-124 AKT serine/threonine kinase 1 Homo sapiens 155-158 23337206-10 2013 As a site of action of indoxyl sulfate on EPO signaling, indoxyl sulfate attenuated EPO-induced tyrosine phosphorylation of EPO receptor (EPOR) in HUVECs. Indican 23-38 erythropoietin Homo sapiens 42-45 23337206-10 2013 As a site of action of indoxyl sulfate on EPO signaling, indoxyl sulfate attenuated EPO-induced tyrosine phosphorylation of EPO receptor (EPOR) in HUVECs. Indican 23-38 erythropoietin receptor Homo sapiens 84-136 23337206-10 2013 As a site of action of indoxyl sulfate on EPO signaling, indoxyl sulfate attenuated EPO-induced tyrosine phosphorylation of EPO receptor (EPOR) in HUVECs. Indican 23-38 erythropoietin receptor Homo sapiens 138-142 23337206-10 2013 As a site of action of indoxyl sulfate on EPO signaling, indoxyl sulfate attenuated EPO-induced tyrosine phosphorylation of EPO receptor (EPOR) in HUVECs. Indican 57-72 erythropoietin Homo sapiens 42-45 23337206-10 2013 As a site of action of indoxyl sulfate on EPO signaling, indoxyl sulfate attenuated EPO-induced tyrosine phosphorylation of EPO receptor (EPOR) in HUVECs. Indican 57-72 erythropoietin receptor Homo sapiens 84-136 23337206-10 2013 As a site of action of indoxyl sulfate on EPO signaling, indoxyl sulfate attenuated EPO-induced tyrosine phosphorylation of EPO receptor (EPOR) in HUVECs. Indican 57-72 erythropoietin receptor Homo sapiens 138-142 23337206-11 2013 CONCLUSIONS: Indoxyl sulfate negatively regulates the EPOR-Akt pathway in endothelial cells, and might contribute to EPO resistance and endothelial dysfunction in patients with CKD. Indican 13-28 erythropoietin receptor Homo sapiens 54-58 23337206-11 2013 CONCLUSIONS: Indoxyl sulfate negatively regulates the EPOR-Akt pathway in endothelial cells, and might contribute to EPO resistance and endothelial dysfunction in patients with CKD. Indican 13-28 AKT serine/threonine kinase 1 Homo sapiens 59-62 23337206-11 2013 CONCLUSIONS: Indoxyl sulfate negatively regulates the EPOR-Akt pathway in endothelial cells, and might contribute to EPO resistance and endothelial dysfunction in patients with CKD. Indican 13-28 erythropoietin Homo sapiens 54-57 23190519-8 2012 In addition, the expression of MRP2 mRNA tended to decrease in cells treated with CMPF, indole-3-acetic acid, or 3-indoxyl sulfate. Indican 113-130 ATP binding cassette subfamily C member 2 Homo sapiens 31-35 22781707-0 2012 Indoxyl sulfate enhances angiotensin II signaling through upregulation of epidermal growth factor receptor expression in vascular smooth muscle cells. Indican 0-15 angiotensinogen Homo sapiens 25-39 22781707-0 2012 Indoxyl sulfate enhances angiotensin II signaling through upregulation of epidermal growth factor receptor expression in vascular smooth muscle cells. Indican 0-15 epidermal growth factor receptor Homo sapiens 74-106 22781707-3 2012 The present study examines whether indoxyl sulfate enhances angiotensin II (Ang II) signaling because serum levels of Ang II are elevated in patients with CKD. Indican 35-50 angiotensinogen Homo sapiens 60-74 22781707-3 2012 The present study examines whether indoxyl sulfate enhances angiotensin II (Ang II) signaling because serum levels of Ang II are elevated in patients with CKD. Indican 35-50 angiotensinogen Homo sapiens 76-82 22781707-3 2012 The present study examines whether indoxyl sulfate enhances angiotensin II (Ang II) signaling because serum levels of Ang II are elevated in patients with CKD. Indican 35-50 angiotensinogen Homo sapiens 118-124 22781707-4 2012 MAIN METHODS: The effect of indoxyl sulfate and Ang II on phosphorylation of ERK and epidermal growth factor receptor (EGFR), and migration were determined using VSMCs. Indican 28-43 mitogen-activated protein kinase 1 Homo sapiens 77-80 22781707-4 2012 MAIN METHODS: The effect of indoxyl sulfate and Ang II on phosphorylation of ERK and epidermal growth factor receptor (EGFR), and migration were determined using VSMCs. Indican 28-43 epidermal growth factor receptor Homo sapiens 85-117 22781707-4 2012 MAIN METHODS: The effect of indoxyl sulfate and Ang II on phosphorylation of ERK and epidermal growth factor receptor (EGFR), and migration were determined using VSMCs. Indican 28-43 epidermal growth factor receptor Homo sapiens 119-123 22781707-5 2012 The expression of EGFR was determined using not only VSMCs but also artery of normal, uremic, and indoxyl sulfate-administrated uremic rats. Indican 98-113 epidermal growth factor receptor Rattus norvegicus 18-22 22781707-6 2012 KEY FINDINGS: Ang II-dependent phosphorylation of ERK and EGFR, and migration of VSMCs were augmented by a prior 24-h incubation with indoxyl sulfate even in the absence of indoxyl sulfate during Ang II stimulation. Indican 134-149 angiotensinogen Homo sapiens 14-20 22781707-6 2012 KEY FINDINGS: Ang II-dependent phosphorylation of ERK and EGFR, and migration of VSMCs were augmented by a prior 24-h incubation with indoxyl sulfate even in the absence of indoxyl sulfate during Ang II stimulation. Indican 134-149 mitogen-activated protein kinase 1 Homo sapiens 50-53 22781707-6 2012 KEY FINDINGS: Ang II-dependent phosphorylation of ERK and EGFR, and migration of VSMCs were augmented by a prior 24-h incubation with indoxyl sulfate even in the absence of indoxyl sulfate during Ang II stimulation. Indican 134-149 epidermal growth factor receptor Homo sapiens 58-62 22781707-6 2012 KEY FINDINGS: Ang II-dependent phosphorylation of ERK and EGFR, and migration of VSMCs were augmented by a prior 24-h incubation with indoxyl sulfate even in the absence of indoxyl sulfate during Ang II stimulation. Indican 134-149 angiotensinogen Homo sapiens 196-202 22781707-7 2012 The expression of EGFR was increased in indoxyl sulfate-stimulated cultured VSMCs. Indican 40-55 epidermal growth factor receptor Homo sapiens 18-22 22781707-8 2012 In arterial VSMCs of rats, serum levels of indoxyl sulfate reflected the expression level of EGFR. Indican 43-58 epidermal growth factor receptor Rattus norvegicus 93-97 22781707-9 2012 The upregulated EGFR expression by indoxyl sulfate was suppressed by the antioxidant, N-acetylcysteine. Indican 35-50 epidermal growth factor receptor Homo sapiens 16-20 22781707-10 2012 An EGFR inhibitor, AG1478, repressed the enhancement of Ang II-induced cellular effects by indoxyl sulfate. Indican 91-106 epidermal growth factor receptor Homo sapiens 3-7 22781707-10 2012 An EGFR inhibitor, AG1478, repressed the enhancement of Ang II-induced cellular effects by indoxyl sulfate. Indican 91-106 angiotensinogen Homo sapiens 56-62 22781707-11 2012 Taken together, these findings indicate that indoxyl sulfate enhances Ang II signaling through reactive oxygen species-induced EGFR expression. Indican 45-60 angiotensinogen Homo sapiens 70-76 22781707-11 2012 Taken together, these findings indicate that indoxyl sulfate enhances Ang II signaling through reactive oxygen species-induced EGFR expression. Indican 45-60 epidermal growth factor receptor Homo sapiens 127-131 22781707-12 2012 SIGNIFICANCE: The actions of indoxyl sulfate including crosstalk with Ang II signaling may be closely involved in the pathogenesis of CKD associated with arteriosclerosis. Indican 29-44 angiogenin Homo sapiens 70-73 22200425-3 2012 Indoxyl sulfate is taken up by proximal tubular cells through organic anion transporters (OAT1, OAT3), and it induces reactive oxygen species (ROS) with impairment of cellular antioxidative system. Indican 0-15 solute carrier family 22 member 6 Rattus norvegicus 90-94 22513409-0 2012 Interaction between two sulfate-conjugated uremic toxins, p-cresyl sulfate and indoxyl sulfate, during binding with human serum albumin. Indican 79-94 albumin Homo sapiens 122-135 22200419-9 2012 Our work also indicated a possible connection between IS and the desensitization of the oxygen-sensing mechanism in erythropoietin-producing cells, which may partly explain inadequate erythropoietin production in hypoxic kidneys of end-stage renal disease patients. Indican 54-56 erythropoietin Homo sapiens 116-130 22200419-9 2012 Our work also indicated a possible connection between IS and the desensitization of the oxygen-sensing mechanism in erythropoietin-producing cells, which may partly explain inadequate erythropoietin production in hypoxic kidneys of end-stage renal disease patients. Indican 54-56 erythropoietin Homo sapiens 184-198 22555846-0 2012 Indoxyl sulfate promotes vascular smooth muscle cell senescence with upregulation of p53, p21, and prelamin A through oxidative stress. Indican 0-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 85-88 22555846-0 2012 Indoxyl sulfate promotes vascular smooth muscle cell senescence with upregulation of p53, p21, and prelamin A through oxidative stress. Indican 0-15 KRAS proto-oncogene, GTPase Rattus norvegicus 90-93 22326498-0 2012 Indoxyl sulfate upregulates renal expression of MCP-1 via production of ROS and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 0-15 C-C motif chemokine ligand 2 Rattus norvegicus 48-53 22326498-0 2012 Indoxyl sulfate upregulates renal expression of MCP-1 via production of ROS and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 0-15 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 94-103 22326498-0 2012 Indoxyl sulfate upregulates renal expression of MCP-1 via production of ROS and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 0-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 105-108 22326498-0 2012 Indoxyl sulfate upregulates renal expression of MCP-1 via production of ROS and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 0-15 Eph receptor B1 Rattus norvegicus 110-113 22326498-0 2012 Indoxyl sulfate upregulates renal expression of MCP-1 via production of ROS and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 0-15 mitogen-activated protein kinase 8 Rattus norvegicus 119-122 22326498-2 2012 The present study examined whether indoxyl sulfate, a uremic toxin, regulates renal expression of MCP-1. Indican 35-50 C-C motif chemokine ligand 2 Rattus norvegicus 98-103 22326498-3 2012 MAIN METHODS: The effect of indoxyl sulfate on the expression of MCP-1 was determined using human proximal tubular cells (HK-2 cells) and following animals: (1) Dahl salt-resistant normotensive rats (DN), (2) Dahl salt-resistant normotensive indoxyl sulfate-administered rats (DN+IS), (3) Dahl salt-sensitive hypertensive rats (DH), and (4) Dahl salt-sensitive hypertensive indoxyl sulfate-administered rats (DH+IS). Indican 28-43 C-C motif chemokine ligand 2 Homo sapiens 65-70 22326498-6 2012 Immunohistochemistry demonstrated the stimulatory effects of indoxyl sulfate on MCP-1 expression and monocyte/macrophage infiltration in the kidneys. Indican 61-76 C-C motif chemokine ligand 2 Rattus norvegicus 80-85 22326498-7 2012 Indoxyl sulfate upregulated mRNA and protein expression of MCP-1 in HK-2 cells. Indican 0-15 chemokine (C-C motif) ligand 2 Mus musculus 59-64 22326498-8 2012 Indoxyl sulfate induced activation of ERK, p38, and JNK as well as of NF-kappaB and p53 in HK-2 cells. Indican 0-15 Eph receptor B1 Rattus norvegicus 38-41 22326498-8 2012 Indoxyl sulfate induced activation of ERK, p38, and JNK as well as of NF-kappaB and p53 in HK-2 cells. Indican 0-15 mitogen activated protein kinase 14 Rattus norvegicus 43-46 22326498-8 2012 Indoxyl sulfate induced activation of ERK, p38, and JNK as well as of NF-kappaB and p53 in HK-2 cells. Indican 0-15 mitogen-activated protein kinase 8 Rattus norvegicus 52-55 22326498-8 2012 Indoxyl sulfate induced activation of ERK, p38, and JNK as well as of NF-kappaB and p53 in HK-2 cells. Indican 0-15 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 70-79 22326498-8 2012 Indoxyl sulfate induced activation of ERK, p38, and JNK as well as of NF-kappaB and p53 in HK-2 cells. Indican 0-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 84-87 22326498-9 2012 An antioxidant, and inhibitors of NF-kappaB, p53, ERK pathway (MEK1/2), and JNK suppressed indoxyl sulfate-induced mRNA expression of MCP-1 in HK-2 cells. Indican 91-106 nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105 Mus musculus 34-43 22326498-9 2012 An antioxidant, and inhibitors of NF-kappaB, p53, ERK pathway (MEK1/2), and JNK suppressed indoxyl sulfate-induced mRNA expression of MCP-1 in HK-2 cells. Indican 91-106 transformation related protein 53, pseudogene Mus musculus 45-48 22326498-9 2012 An antioxidant, and inhibitors of NF-kappaB, p53, ERK pathway (MEK1/2), and JNK suppressed indoxyl sulfate-induced mRNA expression of MCP-1 in HK-2 cells. Indican 91-106 mitogen-activated protein kinase 1 Mus musculus 50-53 22326498-9 2012 An antioxidant, and inhibitors of NF-kappaB, p53, ERK pathway (MEK1/2), and JNK suppressed indoxyl sulfate-induced mRNA expression of MCP-1 in HK-2 cells. Indican 91-106 mitogen-activated protein kinase kinase 1 Mus musculus 63-69 22326498-9 2012 An antioxidant, and inhibitors of NF-kappaB, p53, ERK pathway (MEK1/2), and JNK suppressed indoxyl sulfate-induced mRNA expression of MCP-1 in HK-2 cells. Indican 91-106 mitogen-activated protein kinase 8 Mus musculus 76-79 22326498-9 2012 An antioxidant, and inhibitors of NF-kappaB, p53, ERK pathway (MEK1/2), and JNK suppressed indoxyl sulfate-induced mRNA expression of MCP-1 in HK-2 cells. Indican 91-106 chemokine (C-C motif) ligand 2 Mus musculus 134-139 22326498-10 2012 SIGNIFICANCE: Indoxyl sulfate upregulates renal expression of MCP-1 through production of reactive oxygen species (ROS), and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 14-29 C-C motif chemokine ligand 2 Rattus norvegicus 62-67 22326498-10 2012 SIGNIFICANCE: Indoxyl sulfate upregulates renal expression of MCP-1 through production of reactive oxygen species (ROS), and activation of NF-kappaB, p53, ERK, and JNK in proximal tubular cells. Indican 14-29 mitogen-activated protein kinase 8 Rattus norvegicus 164-167 22326498-11 2012 Thus, accumulation of indoxyl sulfate in chronic kidney disease might be involved in the pathogenesis of tubulointerstitial injury through induction of MCP-1 in the kidneys. Indican 22-37 C-C motif chemokine ligand 2 Rattus norvegicus 152-157 22237753-3 2012 Here we investigated the effects and possible mechanisms by which Klotho expression is regulated during uremia in uninephrectomized B-6 mice given the uremic toxins indoxyl sulfate or p-cresyl sulfate. Indican 165-180 klotho Mus musculus 66-72 22237753-5 2012 Injections of indoxyl sulfate or p-cresyl sulfate increased their serum concentrations, kidney fibrosis, CpG hypermethylation of the Klotho gene, and decreased Klotho expression in renal tubules of these mice. Indican 14-29 klotho Mus musculus 133-139 22237753-5 2012 Injections of indoxyl sulfate or p-cresyl sulfate increased their serum concentrations, kidney fibrosis, CpG hypermethylation of the Klotho gene, and decreased Klotho expression in renal tubules of these mice. Indican 14-29 klotho Mus musculus 160-166 22889746-0 2012 Stat3 contributes to indoxyl sulfate-induced inflammatory and fibrotic gene expression and cellular senescence. Indican 21-36 signal transducer and activator of transcription 3 Rattus norvegicus 0-5 22889746-2 2012 Indoxyl sulfate, a uremic toxin, induces renal fibrosis through expression of transforming growth factor-beta(1) (TGF-beta(1)) in proximal tubular cells. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 78-112 22889746-2 2012 Indoxyl sulfate, a uremic toxin, induces renal fibrosis through expression of transforming growth factor-beta(1) (TGF-beta(1)) in proximal tubular cells. Indican 0-15 transforming growth factor, beta 1 Rattus norvegicus 114-125 22889746-3 2012 The present study aimed to determine whether Stat3 is involved in indoxyl sulfate-induced dysfunction of proximal tubular cells. Indican 66-81 signal transducer and activator of transcription 3 Rattus norvegicus 45-50 22889746-7 2012 Administration of AST-120, which reduces serum level of indoxyl sulfate, to subtotally nephrectomized rats reduced the immunostaining of phosphorylated Stat3 in the renal tubules. Indican 56-71 signal transducer and activator of transcription 3 Rattus norvegicus 152-157 22889746-8 2012 Indoxyl sulfate induced phosphorylation of Stat3 in HK-2 cells. Indican 0-15 signal transducer and activator of transcription 3 Rattus norvegicus 43-48 22889746-9 2012 Stat3 small interfering RNA suppressed indoxyl sulfate-induced expression of an inflammation marker gene (monocyte chemotactic protein-1), fibrosis marker genes (TGF-beta(1), alpha-smooth muscle actin) and a subunit of nuclear factor-kB (p65), and attenuated a cellular senescence marker, senescence-associated beta-galactosidase activity. Indican 39-54 signal transducer and activator of transcription 3 Rattus norvegicus 0-5 22889746-9 2012 Stat3 small interfering RNA suppressed indoxyl sulfate-induced expression of an inflammation marker gene (monocyte chemotactic protein-1), fibrosis marker genes (TGF-beta(1), alpha-smooth muscle actin) and a subunit of nuclear factor-kB (p65), and attenuated a cellular senescence marker, senescence-associated beta-galactosidase activity. Indican 39-54 C-C motif chemokine ligand 2 Rattus norvegicus 106-136 22889746-9 2012 Stat3 small interfering RNA suppressed indoxyl sulfate-induced expression of an inflammation marker gene (monocyte chemotactic protein-1), fibrosis marker genes (TGF-beta(1), alpha-smooth muscle actin) and a subunit of nuclear factor-kB (p65), and attenuated a cellular senescence marker, senescence-associated beta-galactosidase activity. Indican 39-54 transforming growth factor, beta 1 Rattus norvegicus 162-173 22889746-9 2012 Stat3 small interfering RNA suppressed indoxyl sulfate-induced expression of an inflammation marker gene (monocyte chemotactic protein-1), fibrosis marker genes (TGF-beta(1), alpha-smooth muscle actin) and a subunit of nuclear factor-kB (p65), and attenuated a cellular senescence marker, senescence-associated beta-galactosidase activity. Indican 39-54 synaptotagmin 1 Rattus norvegicus 238-241 22889746-9 2012 Stat3 small interfering RNA suppressed indoxyl sulfate-induced expression of an inflammation marker gene (monocyte chemotactic protein-1), fibrosis marker genes (TGF-beta(1), alpha-smooth muscle actin) and a subunit of nuclear factor-kB (p65), and attenuated a cellular senescence marker, senescence-associated beta-galactosidase activity. Indican 39-54 galactosidase, beta 1 Rattus norvegicus 311-329 22889746-10 2012 CONCLUSIONS: Stat3 is involved in indoxyl sulfate-induced inflammatory and fibrotic gene expression and cellular senescence in proximal tubular cells. Indican 34-49 signal transducer and activator of transcription 3 Rattus norvegicus 13-18 22200421-0 2012 Indoxyl sulfate induces endothelial cell senescence by increasing reactive oxygen species production and p53 activity. Indican 0-15 tumor protein p53 Homo sapiens 105-108 22200425-3 2012 Indoxyl sulfate is taken up by proximal tubular cells through organic anion transporters (OAT1, OAT3), and it induces reactive oxygen species (ROS) with impairment of cellular antioxidative system. Indican 0-15 solute carrier family 22 member 8 Rattus norvegicus 96-100 22200425-6 2012 Administration of indoxyl sulfate to hypertensive rats reduces renal expression of Klotho and promotes cell senescence, with expression of senescence-associated beta-galactosidase, p53, p21, p16, and retinoblastoma protein, accompanied by kidney fibrosis. Indican 18-33 Klotho Rattus norvegicus 83-89 22200425-6 2012 Administration of indoxyl sulfate to hypertensive rats reduces renal expression of Klotho and promotes cell senescence, with expression of senescence-associated beta-galactosidase, p53, p21, p16, and retinoblastoma protein, accompanied by kidney fibrosis. Indican 18-33 galactosidase, beta 1 Rattus norvegicus 161-179 22200425-6 2012 Administration of indoxyl sulfate to hypertensive rats reduces renal expression of Klotho and promotes cell senescence, with expression of senescence-associated beta-galactosidase, p53, p21, p16, and retinoblastoma protein, accompanied by kidney fibrosis. Indican 18-33 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 181-184 22200425-6 2012 Administration of indoxyl sulfate to hypertensive rats reduces renal expression of Klotho and promotes cell senescence, with expression of senescence-associated beta-galactosidase, p53, p21, p16, and retinoblastoma protein, accompanied by kidney fibrosis. Indican 18-33 KRAS proto-oncogene, GTPase Rattus norvegicus 186-189 22200425-6 2012 Administration of indoxyl sulfate to hypertensive rats reduces renal expression of Klotho and promotes cell senescence, with expression of senescence-associated beta-galactosidase, p53, p21, p16, and retinoblastoma protein, accompanied by kidney fibrosis. Indican 18-33 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 191-194 22200425-7 2012 Indoxyl sulfate downregulates Klotho expression in the kidneys through production of ROS and activation of nuclear factor kappa B in proximal tubular cells. Indican 0-15 Klotho Rattus norvegicus 30-36 21832251-9 2011 NF-kappaB inhibitors partially alleviated indoxyl sulfate-induced inhibition of cellular proliferation. Indican 42-57 nuclear factor kappa B subunit 1 Homo sapiens 0-9 21832251-10 2011 NF-kappaB p65 siRNA-transfected cells showed less proliferation in the presence of indoxyl sulfate than control cells. Indican 83-98 nuclear factor kappa B subunit 1 Homo sapiens 0-9 21832251-10 2011 NF-kappaB p65 siRNA-transfected cells showed less proliferation in the presence of indoxyl sulfate than control cells. Indican 83-98 synaptotagmin 1 Rattus norvegicus 10-13 21832251-0 2011 NF-kappaB plays an important role in indoxyl sulfate-induced cellular senescence, fibrotic gene expression, and inhibition of proliferation in proximal tubular cells. Indican 37-52 nuclear factor kappa B subunit 1 Homo sapiens 0-9 21832251-13 2011 Taken together, NF-kappaB plays an important role in indoxyl sulfate-induced cellular senescence, fibrotic gene expression, and inhibition of proliferation in proximal tubular cells. Indican 53-68 nuclear factor kappa B subunit 1 Homo sapiens 16-25 21832251-14 2011 More notably, indoxyl sulfate accelerates proximal tubular cell senescence with progression of CRF through reactive oxygen species-NF-kappaB-p53 pathway. Indican 14-29 nuclear factor kappa B subunit 1 Homo sapiens 131-140 21832251-1 2011 We previously demonstrated that indoxyl sulfate induces senescence and dysfunction of proximal tubular cells by activating p53 expression. Indican 32-47 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 123-126 21832251-14 2011 More notably, indoxyl sulfate accelerates proximal tubular cell senescence with progression of CRF through reactive oxygen species-NF-kappaB-p53 pathway. Indican 14-29 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 141-144 21832251-3 2011 The present study examines whether activation (phosphorylation) of NF-kappaB by indoxyl sulfate promotes senescence and dysfunction in human proximal tubular cells (HK-2 cells). Indican 80-95 nuclear factor kappa B subunit 1 Homo sapiens 67-76 21863063-0 2011 Indoxyl sulfate, a representative uremic toxin, suppresses erythropoietin production in a HIF-dependent manner. Indican 0-15 erythropoietin Homo sapiens 59-73 21832251-4 2011 Indoxyl sulfate induced phosphorylation of NF-kappaB p65 on Ser-276, which was suppressed by N-acetylcysteine, an antioxidant. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 43-52 21832251-4 2011 Indoxyl sulfate induced phosphorylation of NF-kappaB p65 on Ser-276, which was suppressed by N-acetylcysteine, an antioxidant. Indican 0-15 synaptotagmin 1 Rattus norvegicus 53-56 21832251-5 2011 Furthermore, indoxyl sulfate induced NF-kappaB p65 expression. Indican 13-28 nuclear factor kappa B subunit 1 Homo sapiens 37-46 21832251-5 2011 Furthermore, indoxyl sulfate induced NF-kappaB p65 expression. Indican 13-28 synaptotagmin 1 Rattus norvegicus 47-50 21832251-6 2011 Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA). Indican 128-143 nuclear factor kappa B subunit 1 Homo sapiens 14-23 21832251-6 2011 Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA). Indican 128-143 nuclear factor kappa B subunit 1 Homo sapiens 73-82 21832251-6 2011 Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA). Indican 128-143 synaptotagmin 1 Rattus norvegicus 83-86 21832251-6 2011 Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA). Indican 128-143 galactosidase, beta 1 Rattus norvegicus 174-192 21832251-6 2011 Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA). Indican 128-143 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 220-223 21832251-6 2011 Inhibitors of NF-kappaB (pyrrolidine dithiocarbamate and isohelenin) and NF-kappaB p65 small interfering RNA (siRNA) suppressed indoxyl sulfate-induced senescence-associated beta-galactosidase activity and expression of p53, transforming growth factor (TGF)-beta1, and alpha-smoothe muscle actin (SMA). Indican 128-143 transforming growth factor, beta 1 Rattus norvegicus 225-263 21832251-7 2011 The induction of p53 expression and p53 promoter activity by indoxyl sulfate were inhibited by pifithrin-alpha, p-nitro, an inhibitor of p53, whereas p53-transfected cells showed enhanced p53 promoter activity. Indican 61-76 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 17-20 21832251-7 2011 The induction of p53 expression and p53 promoter activity by indoxyl sulfate were inhibited by pifithrin-alpha, p-nitro, an inhibitor of p53, whereas p53-transfected cells showed enhanced p53 promoter activity. Indican 61-76 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 36-39 21832251-7 2011 The induction of p53 expression and p53 promoter activity by indoxyl sulfate were inhibited by pifithrin-alpha, p-nitro, an inhibitor of p53, whereas p53-transfected cells showed enhanced p53 promoter activity. Indican 61-76 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 36-39 21832251-7 2011 The induction of p53 expression and p53 promoter activity by indoxyl sulfate were inhibited by pifithrin-alpha, p-nitro, an inhibitor of p53, whereas p53-transfected cells showed enhanced p53 promoter activity. Indican 61-76 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 36-39 21832251-7 2011 The induction of p53 expression and p53 promoter activity by indoxyl sulfate were inhibited by pifithrin-alpha, p-nitro, an inhibitor of p53, whereas p53-transfected cells showed enhanced p53 promoter activity. Indican 61-76 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 36-39 21832251-8 2011 NF-kappaB inhibitors suppressed indoxyl sulfate-induced p21 expression, whereas NF-kappaB p65 siRNA enhanced its expression. Indican 32-47 nuclear factor kappa B subunit 1 Homo sapiens 0-9 21832251-8 2011 NF-kappaB inhibitors suppressed indoxyl sulfate-induced p21 expression, whereas NF-kappaB p65 siRNA enhanced its expression. Indican 32-47 KRAS proto-oncogene, GTPase Rattus norvegicus 56-59 21611756-3 2011 Our recent research provides novel molecular and functional evidence that indoxyl sulfate, an anionic uremic toxin, undergoes efflux transport at the BBB via OAT3 and creatinine, a uremic guanidino compound, undergoes efflux transport at the BCSFB via OCT3. Indican 74-89 solute carrier family 22 member 8 Homo sapiens 158-162 21611756-3 2011 Our recent research provides novel molecular and functional evidence that indoxyl sulfate, an anionic uremic toxin, undergoes efflux transport at the BBB via OAT3 and creatinine, a uremic guanidino compound, undergoes efflux transport at the BCSFB via OCT3. Indican 74-89 solute carrier family 22 member 3 Homo sapiens 252-256 21621512-0 2011 Nitric oxide counters the inhibitory effects of uremic toxin indoxyl sulfate on endothelial cells by governing ERK MAP kinase and myosin light chain activation. Indican 61-76 modulator of VRAC current 1 Homo sapiens 130-148 21245127-9 2011 AST-120 significantly decreased necrotic areas and lessened aortic deposition of the uremic toxin indoxyl sulfate without affecting lesional macrophage or collagen content. Indican 98-113 solute carrier family 17 (anion/sugar transporter), member 5 Mus musculus 0-3 21476605-4 2011 Three metabolites, indoxyl sulfate, kynurenine, and xanthurenic acid, were elevated in the plasma and interacted strongly and directly with Oat1 in vitro with IC50 of 18, 12, and 50 muM, respectively. Indican 19-34 solute carrier family 22 (organic anion transporter), member 6 Mus musculus 140-144 21426504-6 2011 Indoxyl sulfate effects were associated with a dose-dependent induction of intracellular reactive oxygen species and up-regulation of p21 and p27 protein expression. Indican 0-15 H3 histone pseudogene 16 Homo sapiens 134-137 21426504-6 2011 Indoxyl sulfate effects were associated with a dose-dependent induction of intracellular reactive oxygen species and up-regulation of p21 and p27 protein expression. Indican 0-15 interferon alpha inducible protein 27 Homo sapiens 142-145 21811066-0 2011 Clopidogrel effectively suppresses endothelial microparticle generation induced by indoxyl sulfate via inhibition of the p38 mitogen-activated protein kinase pathway. Indican 83-98 mitogen-activated protein kinase 14 Homo sapiens 121-124 21389697-0 2011 Indoxyl sulfate downregulates renal expression of Klotho through production of ROS and activation of nuclear factor-kB. Indican 0-15 Klotho Rattus norvegicus 50-56 21389697-2 2011 The present study aimed to examine whether renal expression of Klotho is regulated by indoxyl sulfate, a uremic toxin, using rat kidneys and human proximal tubular cells (HK-2). Indican 86-101 Klotho Rattus norvegicus 63-69 21389697-3 2011 METHODS: The effect of indoxyl sulfate on renal expression of Klotho was examined using (1) Dahl salt-resistant normotensive rats (DN), (2) Dahl salt-resistant normotensive indoxyl sulfate-administered rats (DN+IS), (3) Dahl salt-sensitive hypertensive rats (DH), and (4) Dahl salt-sensitive hypertensive indoxyl sulfate-administered rats (DH+IS). Indican 23-38 Klotho Rattus norvegicus 62-68 21389697-3 2011 METHODS: The effect of indoxyl sulfate on renal expression of Klotho was examined using (1) Dahl salt-resistant normotensive rats (DN), (2) Dahl salt-resistant normotensive indoxyl sulfate-administered rats (DN+IS), (3) Dahl salt-sensitive hypertensive rats (DH), and (4) Dahl salt-sensitive hypertensive indoxyl sulfate-administered rats (DH+IS). Indican 173-188 Klotho Rattus norvegicus 62-68 21389697-3 2011 METHODS: The effect of indoxyl sulfate on renal expression of Klotho was examined using (1) Dahl salt-resistant normotensive rats (DN), (2) Dahl salt-resistant normotensive indoxyl sulfate-administered rats (DN+IS), (3) Dahl salt-sensitive hypertensive rats (DH), and (4) Dahl salt-sensitive hypertensive indoxyl sulfate-administered rats (DH+IS). Indican 173-188 Klotho Rattus norvegicus 62-68 21389697-4 2011 The effects of indoxyl sulfate, inhibitors of nuclear factor-kappaB (NF-kappaB) and an antioxidant on the expression of Klotho in HK-2 cells were examined. Indican 15-30 Klotho Rattus norvegicus 120-126 21389697-6 2011 Indoxyl sulfate suppressed the expression of Klotho mRNA and protein in HK-2 cells, whereas an antioxidant, N-acetylcysteine, and NF-kappaB inhibitors, pyrrolidine dithiocarbamate and isohelenin, alleviated these effects. Indican 0-15 Klotho Rattus norvegicus 45-51 21389697-7 2011 CONCLUSIONS: Indoxyl sulfate downregulates Klotho expression in kidneys through production of reactive oxygen species and activation of NF-kappaB in proximal tubular cells. Indican 13-28 Klotho Rattus norvegicus 43-49 21389697-8 2011 Indoxyl sulfate may be involved in reduced renal expression of Klotho in CKD. Indican 0-15 Klotho Rattus norvegicus 63-69 21811066-3 2011 METHODS: CD31+CD42-EMP counts were measured by flow cytometry in supernatants of HUVECs incubated with indoxyl sulfate. Indican 103-118 platelet and endothelial cell adhesion molecule 1 Homo sapiens 9-13 21811066-6 2011 RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38. Indican 13-28 latexin Homo sapiens 109-112 21811066-6 2011 RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38. Indican 150-165 latexin Homo sapiens 109-112 21811066-6 2011 RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38. Indican 150-165 mitogen-activated protein kinase 14 Homo sapiens 218-221 21811066-6 2011 RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38. Indican 150-165 mitogen-activated protein kinase 14 Homo sapiens 406-409 21811066-6 2011 RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38. Indican 274-289 latexin Homo sapiens 109-112 21811066-6 2011 RESULTS: (1) Indoxyl sulfate induced EMP release in HUVECs in a dose-dependent fashion; (2) all drugs (10-50 muM) inhibited EMP generation induced by indoxyl sulfate, with clopidogrel being the most effective; (3) the p38 MAPK inhibitor suppressed EMP generation induced by indoxyl sulfate, and (4) clopidogrel significantly suppressed MAPK signaling activated by indoxyl sulfate, with the most potency on p38. Indican 274-289 latexin Homo sapiens 109-112 21811066-7 2011 CONCLUSION: The p38 signaling involves EMP generation induced by indoxyl sulfate and is effectively suppressed by clopidogrel. Indican 65-80 mitogen-activated protein kinase 14 Homo sapiens 16-19 20720180-5 2010 Indoxyl sulfate evoked reactive oxygen species (ROS), and the antioxidant N-acetylcysteine inhibited indoxyl sulfate-induced p53 expression and phosphorylation, as well as indoxyl sulfate-induced alpha-SMA expression. Indican 0-15 actin gamma 2, smooth muscle Rattus norvegicus 196-205 20937831-0 2010 Indoxyl sulfate induces leukocyte-endothelial interactions through up-regulation of E-selectin. Indican 0-15 selectin E Homo sapiens 84-94 20937831-3 2010 Pretreatment of human umbilical vein endothelial cells (HUVEC) with indoxyl sulfate significantly enhanced the adhesion of human monocytic cells (THP-1 cell line) to TNF-alpha-activated HUVEC under physiological flow conditions. Indican 68-83 GLI family zinc finger 2 Homo sapiens 146-151 20937831-3 2010 Pretreatment of human umbilical vein endothelial cells (HUVEC) with indoxyl sulfate significantly enhanced the adhesion of human monocytic cells (THP-1 cell line) to TNF-alpha-activated HUVEC under physiological flow conditions. Indican 68-83 tumor necrosis factor Homo sapiens 166-175 20937831-4 2010 Treatment with indoxyl sulfate enhanced the expression level of E-selectin, but not that of ICAM-1 or VCAM-1, in HUVEC. Indican 15-30 selectin E Homo sapiens 64-74 20937831-5 2010 Indoxyl sulfate treatment enhanced the activation of JNK, p38 MAPK, and NF-kappaB in TNF-alpha-activated HUVEC. Indican 0-15 mitogen-activated protein kinase 8 Homo sapiens 53-56 20937831-5 2010 Indoxyl sulfate treatment enhanced the activation of JNK, p38 MAPK, and NF-kappaB in TNF-alpha-activated HUVEC. Indican 0-15 mitogen-activated protein kinase 14 Homo sapiens 58-61 20937831-5 2010 Indoxyl sulfate treatment enhanced the activation of JNK, p38 MAPK, and NF-kappaB in TNF-alpha-activated HUVEC. Indican 0-15 tumor necrosis factor Homo sapiens 85-94 20937831-6 2010 Inhibitors of JNK and NF-kappaB attenuated indoxyl sulfate-induced E-selectin expression in HUVEC and subsequent THP-1 adhesion. Indican 43-58 mitogen-activated protein kinase 8 Homo sapiens 14-17 20937831-6 2010 Inhibitors of JNK and NF-kappaB attenuated indoxyl sulfate-induced E-selectin expression in HUVEC and subsequent THP-1 adhesion. Indican 43-58 selectin E Homo sapiens 67-77 20937831-6 2010 Inhibitors of JNK and NF-kappaB attenuated indoxyl sulfate-induced E-selectin expression in HUVEC and subsequent THP-1 adhesion. Indican 43-58 GLI family zinc finger 2 Homo sapiens 113-118 20937831-7 2010 Furthermore, treatment with the NAD(P)H oxidase inhibitor apocynin and the glutathione donor N-acetylcysteine inhibited indoxyl sulfate-induced enhancement of THP-1 adhesion to HUVEC. Indican 120-135 GLI family zinc finger 2 Homo sapiens 159-164 20937831-9 2010 Indoxyl sulfate-induced leukocyte adhesion to the femoral artery was significantly reduced by anti-E-selectin antibody treatment. Indican 0-15 selectin E Homo sapiens 99-109 20937831-10 2010 These findings suggest that indoxyl sulfate enhances leukocyte-endothelial interactions through up-regulation of E-selectin, presumably via the JNK- and NF-kappaB-dependent pathway. Indican 28-43 selectin E Homo sapiens 113-123 20937831-10 2010 These findings suggest that indoxyl sulfate enhances leukocyte-endothelial interactions through up-regulation of E-selectin, presumably via the JNK- and NF-kappaB-dependent pathway. Indican 28-43 mitogen-activated protein kinase 8 Homo sapiens 144-148 21195930-8 2011 CONCLUSION: Administration of indoxyl sulfate to hypertensive rats reduced renal expression of klotho and promoted cell senescence with expression of senescence-related proteins, such as p16(INK4a), p21(WAF1/CIP1), p53, and Rb, which was accompanied by renal fibrosis. Indican 30-45 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 187-190 21195930-8 2011 CONCLUSION: Administration of indoxyl sulfate to hypertensive rats reduced renal expression of klotho and promoted cell senescence with expression of senescence-related proteins, such as p16(INK4a), p21(WAF1/CIP1), p53, and Rb, which was accompanied by renal fibrosis. Indican 30-45 cyclin-dependent kinase inhibitor 2A Rattus norvegicus 191-196 21195930-8 2011 CONCLUSION: Administration of indoxyl sulfate to hypertensive rats reduced renal expression of klotho and promoted cell senescence with expression of senescence-related proteins, such as p16(INK4a), p21(WAF1/CIP1), p53, and Rb, which was accompanied by renal fibrosis. Indican 30-45 KRAS proto-oncogene, GTPase Rattus norvegicus 199-202 21195930-8 2011 CONCLUSION: Administration of indoxyl sulfate to hypertensive rats reduced renal expression of klotho and promoted cell senescence with expression of senescence-related proteins, such as p16(INK4a), p21(WAF1/CIP1), p53, and Rb, which was accompanied by renal fibrosis. Indican 30-45 cyclin-dependent kinase inhibitor 1A Rattus norvegicus 203-212 21195930-8 2011 CONCLUSION: Administration of indoxyl sulfate to hypertensive rats reduced renal expression of klotho and promoted cell senescence with expression of senescence-related proteins, such as p16(INK4a), p21(WAF1/CIP1), p53, and Rb, which was accompanied by renal fibrosis. Indican 30-45 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 215-218 20720180-0 2010 Senescence and dysfunction of proximal tubular cells are associated with activated p53 expression by indoxyl sulfate. Indican 101-116 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 83-86 20720180-3 2010 Indoxyl sulfate inhibited serum-induced cell proliferation and promoted the activation of senescence-associated beta-galactosidase, a marker of cellular senescence, and the expression of alpha-smooth muscle actin (alpha-SMA), a marker of fibrosis, through inducing p53 expression and phosphorylation. Indican 0-15 galactosidase, beta 1 Rattus norvegicus 112-130 20720180-3 2010 Indoxyl sulfate inhibited serum-induced cell proliferation and promoted the activation of senescence-associated beta-galactosidase, a marker of cellular senescence, and the expression of alpha-smooth muscle actin (alpha-SMA), a marker of fibrosis, through inducing p53 expression and phosphorylation. Indican 0-15 actin gamma 2, smooth muscle Rattus norvegicus 187-212 20720180-3 2010 Indoxyl sulfate inhibited serum-induced cell proliferation and promoted the activation of senescence-associated beta-galactosidase, a marker of cellular senescence, and the expression of alpha-smooth muscle actin (alpha-SMA), a marker of fibrosis, through inducing p53 expression and phosphorylation. Indican 0-15 actin gamma 2, smooth muscle Rattus norvegicus 214-223 20720180-3 2010 Indoxyl sulfate inhibited serum-induced cell proliferation and promoted the activation of senescence-associated beta-galactosidase, a marker of cellular senescence, and the expression of alpha-smooth muscle actin (alpha-SMA), a marker of fibrosis, through inducing p53 expression and phosphorylation. Indican 0-15 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 265-268 20720180-5 2010 Indoxyl sulfate evoked reactive oxygen species (ROS), and the antioxidant N-acetylcysteine inhibited indoxyl sulfate-induced p53 expression and phosphorylation, as well as indoxyl sulfate-induced alpha-SMA expression. Indican 101-116 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 125-128 20720180-5 2010 Indoxyl sulfate evoked reactive oxygen species (ROS), and the antioxidant N-acetylcysteine inhibited indoxyl sulfate-induced p53 expression and phosphorylation, as well as indoxyl sulfate-induced alpha-SMA expression. Indican 101-116 actin gamma 2, smooth muscle Rattus norvegicus 196-205 20720180-8 2010 Taken together, these findings indicate that indoxyl sulfate induces the expression and phosphorylation of p53 though ROS production, thus inhibiting cell proliferation and promoting cellular senescence and renal fibrosis. Indican 45-60 Wistar clone pR53P1 p53 pseudogene Rattus norvegicus 107-110 19027976-7 2009 When the patients were stratified by the estimated glomerular filtration rate, serum indoxyl sulfate was elevated in groups with estimated glomerular filtration rates of 60-89 mL/min/1.73 m(2) and below. Indican 85-100 CD59 molecule (CD59 blood group) Homo sapiens 179-184 20870466-5 2010 Indoxyl sulfate was the first principal serum metabolite, which could differentiate CRF from both normal and AST-120-administered CRF rats, followed by hippuric acid, phenyl sulfate and 4-ethylphenyl sulfate. Indican 0-15 solute carrier family 17 member 5 Homo sapiens 109-112 20870466-8 2010 In conclusion, indoxyl sulfate is the best indicator of the effect of AST-120 in CRF rats. Indican 15-30 solute carrier family 17 member 5 Homo sapiens 70-73 20797565-2 2010 The oral sorbent AST-120 reduces the serum levels of indoxyl sulfate in CKD patients by adsorbing indole, a precursor of indoxyl sulfate, in the intestine, and thereby stimulating its excretion in feces. Indican 121-136 solute carrier family 17 member 5 Homo sapiens 17-20 20797565-4 2010 Indoxyl sulfate is taken up by the cells through organic anion transporters (OAT1 and/or OAT3), and induces cellular production of free radicals such as superoxide by activating nicotinamide adenine dinucleotide phosphate oxidase, especially Nox4, thereby impairing the cellular antioxidative system. Indican 0-15 solute carrier family 22 member 6 Homo sapiens 77-81 20797565-4 2010 Indoxyl sulfate is taken up by the cells through organic anion transporters (OAT1 and/or OAT3), and induces cellular production of free radicals such as superoxide by activating nicotinamide adenine dinucleotide phosphate oxidase, especially Nox4, thereby impairing the cellular antioxidative system. Indican 0-15 solute carrier family 22 member 8 Homo sapiens 89-93 20797565-4 2010 Indoxyl sulfate is taken up by the cells through organic anion transporters (OAT1 and/or OAT3), and induces cellular production of free radicals such as superoxide by activating nicotinamide adenine dinucleotide phosphate oxidase, especially Nox4, thereby impairing the cellular antioxidative system. Indican 0-15 NADPH oxidase 4 Homo sapiens 242-246 20797565-6 2010 I proposed the protein metabolite theory, which states that endogenous protein metabolites such as indoxyl sulfate play a significant role in the progression of CKD by increasing expressions of transforming growth factor-beta1, tissue inhibitor of metalloproteinase-1, and proalpha1(I)collagen. Indican 99-114 transforming growth factor beta 1 Homo sapiens 194-226 20797565-11 2010 Therefore, AST-120 may ameliorate the progression of cardiovascular disease as well as of CKD by removing indoxyl sulfate. Indican 106-121 solute carrier family 17 member 5 Homo sapiens 11-14 20229698-9 2010 Indoxyl sulfate stimulates progressive both tubulointerstitial fibrosis and glomerular sclerosis by increasing the expression of transforming growth factor-beta1, a tissue inhibitor of metalloproteinase-1 and proalpha1 (I) collagen, leading to a further loss of nephrons. Indican 0-15 transforming growth factor beta 1 Homo sapiens 129-161 20000589-0 2010 The uremic toxin 3-indoxyl sulfate is a potent endogenous agonist for the human aryl hydrocarbon receptor. Indican 17-34 aryl hydrocarbon receptor Homo sapiens 80-105 20389059-0 2010 Indoxyl sulfate upregulates expression of ICAM-1 and MCP-1 by oxidative stress-induced NF-kappaB activation. Indican 0-15 intercellular adhesion molecule 1 Homo sapiens 42-48 19837111-9 2010 Indoxyl sulfate, a uremic toxin and substrate of OAT1 and OAT3, appears to mediate the progression of AKI evoked by renal ischemia and cisplatin treatment. Indican 0-15 solute carrier family 22 member 6 Homo sapiens 49-53 19837111-9 2010 Indoxyl sulfate, a uremic toxin and substrate of OAT1 and OAT3, appears to mediate the progression of AKI evoked by renal ischemia and cisplatin treatment. Indican 0-15 solute carrier family 22 member 8 Homo sapiens 58-62 20818133-0 2010 Indoxyl sulfate stimulates monocyte chemoattractant protein-1 expression in human umbilical vein endothelial cells by inducing oxidative stress through activation of the NADPH oxidase-nuclear factor-kappaB pathway. Indican 0-15 C-C motif chemokine ligand 2 Homo sapiens 27-61 20797565-2 2010 The oral sorbent AST-120 reduces the serum levels of indoxyl sulfate in CKD patients by adsorbing indole, a precursor of indoxyl sulfate, in the intestine, and thereby stimulating its excretion in feces. Indican 53-68 solute carrier family 17 member 5 Homo sapiens 17-20 20649763-6 2010 Multiple regression analysis shows that indoxyl sulfate correlated negatively with ALP (beta = -1.897, P = 0.042) and BAP (beta = -0.310, P = 0.029), independent of intact PTH; however, indoxyl sulfate did not correlate with TRACP-5b or 8-OHdG. Indican 40-55 alkaline phosphatase, placental Homo sapiens 83-86 20649763-6 2010 Multiple regression analysis shows that indoxyl sulfate correlated negatively with ALP (beta = -1.897, P = 0.042) and BAP (beta = -0.310, P = 0.029), independent of intact PTH; however, indoxyl sulfate did not correlate with TRACP-5b or 8-OHdG. Indican 40-55 acid phosphatase 5, tartrate resistant Homo sapiens 225-233 20047993-4 2010 Indoxyl sulfate stimulated tumour necrosis factor-alpha, interleukin-6 (IL-6), and IL-1beta mRNA expression in THP-1 cells as quantified by RT-PCR. Indican 0-15 interleukin 6 Homo sapiens 57-70 20047993-4 2010 Indoxyl sulfate stimulated tumour necrosis factor-alpha, interleukin-6 (IL-6), and IL-1beta mRNA expression in THP-1 cells as quantified by RT-PCR. Indican 0-15 interleukin 6 Homo sapiens 72-76 20047993-4 2010 Indoxyl sulfate stimulated tumour necrosis factor-alpha, interleukin-6 (IL-6), and IL-1beta mRNA expression in THP-1 cells as quantified by RT-PCR. Indican 0-15 interleukin 1 beta Homo sapiens 83-91 20047993-5 2010 Both p38 (RWJ-67657) and MEK1/2 (U0126) inhibitors suppressed all these effects by IS. Indican 83-85 mitogen-activated protein kinase 14 Homo sapiens 5-8 20047993-5 2010 Both p38 (RWJ-67657) and MEK1/2 (U0126) inhibitors suppressed all these effects by IS. Indican 83-85 mitogen-activated protein kinase kinase 1 Homo sapiens 25-31 20338972-18 2010 IL-6 level was significantly associated with free indoxyl sulfate level. Indican 50-65 interleukin 6 Homo sapiens 0-4 20389059-0 2010 Indoxyl sulfate upregulates expression of ICAM-1 and MCP-1 by oxidative stress-induced NF-kappaB activation. Indican 0-15 C-C motif chemokine ligand 2 Homo sapiens 53-58 20389059-0 2010 Indoxyl sulfate upregulates expression of ICAM-1 and MCP-1 by oxidative stress-induced NF-kappaB activation. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 87-96 20389059-2 2010 The present study aimed to determine whether indoxyl sulfate increases the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) by reactive oxygen species (ROS)-induced activation of nuclear factor-kappaB (NF-kappaB) in vascular endothelial cells. Indican 45-60 intercellular adhesion molecule 1 Homo sapiens 89-122 20389059-2 2010 The present study aimed to determine whether indoxyl sulfate increases the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) by reactive oxygen species (ROS)-induced activation of nuclear factor-kappaB (NF-kappaB) in vascular endothelial cells. Indican 45-60 intercellular adhesion molecule 1 Homo sapiens 124-130 20389059-2 2010 The present study aimed to determine whether indoxyl sulfate increases the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) by reactive oxygen species (ROS)-induced activation of nuclear factor-kappaB (NF-kappaB) in vascular endothelial cells. Indican 45-60 C-C motif chemokine ligand 2 Homo sapiens 136-166 20389059-2 2010 The present study aimed to determine whether indoxyl sulfate increases the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) by reactive oxygen species (ROS)-induced activation of nuclear factor-kappaB (NF-kappaB) in vascular endothelial cells. Indican 45-60 C-C motif chemokine ligand 2 Homo sapiens 168-173 20389059-2 2010 The present study aimed to determine whether indoxyl sulfate increases the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) by reactive oxygen species (ROS)-induced activation of nuclear factor-kappaB (NF-kappaB) in vascular endothelial cells. Indican 45-60 nuclear factor kappa B subunit 1 Homo sapiens 230-251 20389059-2 2010 The present study aimed to determine whether indoxyl sulfate increases the expression of intercellular adhesion molecule-1 (ICAM-1) and monocyte chemotactic protein-1 (MCP-1) by reactive oxygen species (ROS)-induced activation of nuclear factor-kappaB (NF-kappaB) in vascular endothelial cells. Indican 45-60 nuclear factor kappa B subunit 1 Homo sapiens 253-262 20389059-6 2010 RESULTS: Indoxyl sulfate significantly increased the mRNA expression of ICAM-1 and MCP-1 in HUVEC in a time- and concentration-dependent manner. Indican 9-24 intercellular adhesion molecule 1 Homo sapiens 72-78 20389059-6 2010 RESULTS: Indoxyl sulfate significantly increased the mRNA expression of ICAM-1 and MCP-1 in HUVEC in a time- and concentration-dependent manner. Indican 9-24 C-C motif chemokine ligand 2 Homo sapiens 83-88 20389059-7 2010 Inhibitors of NF-kappaB (ammonium pyrrolidinedithiocarbamate and isohelenin) and an antioxidant (N-acetyl-L-cysteine) suppressed the indoxyl sulfate-induced expression of ICAM-1 and MCP-1 in HUVEC. Indican 133-148 nuclear factor kappa B subunit 1 Homo sapiens 14-23 20389059-7 2010 Inhibitors of NF-kappaB (ammonium pyrrolidinedithiocarbamate and isohelenin) and an antioxidant (N-acetyl-L-cysteine) suppressed the indoxyl sulfate-induced expression of ICAM-1 and MCP-1 in HUVEC. Indican 133-148 intercellular adhesion molecule 1 Homo sapiens 171-177 20389059-7 2010 Inhibitors of NF-kappaB (ammonium pyrrolidinedithiocarbamate and isohelenin) and an antioxidant (N-acetyl-L-cysteine) suppressed the indoxyl sulfate-induced expression of ICAM-1 and MCP-1 in HUVEC. Indican 133-148 C-C motif chemokine ligand 2 Homo sapiens 182-187 20389059-8 2010 Indoxyl sulfate increased phospho- NF-kappaB p65 in HUVEC, and N-acetyl-L-cysteine suppressed it. Indican 0-15 nuclear factor kappa B subunit 1 Homo sapiens 35-44 20389059-8 2010 Indoxyl sulfate increased phospho- NF-kappaB p65 in HUVEC, and N-acetyl-L-cysteine suppressed it. Indican 0-15 RELA proto-oncogene, NF-kB subunit Homo sapiens 45-48 20389059-9 2010 CONCLUSIONS: Indoxyl sulfate upregulates the expression of ICAM-1 and MCP-1 by ROS-induced activation of NF-kappaB in vascular endothelial cells. Indican 13-28 intercellular adhesion molecule 1 Homo sapiens 59-65 20389059-9 2010 CONCLUSIONS: Indoxyl sulfate upregulates the expression of ICAM-1 and MCP-1 by ROS-induced activation of NF-kappaB in vascular endothelial cells. Indican 13-28 C-C motif chemokine ligand 2 Homo sapiens 70-75 20389059-9 2010 CONCLUSIONS: Indoxyl sulfate upregulates the expression of ICAM-1 and MCP-1 by ROS-induced activation of NF-kappaB in vascular endothelial cells. Indican 13-28 nuclear factor kappa B subunit 1 Homo sapiens 105-114 20389059-10 2010 Thus, indoxyl sulfate may play an important role in the development of CVD in CKD by increasing the endothelial expression of ICAM-1 and MCP-1. Indican 6-21 intercellular adhesion molecule 1 Homo sapiens 126-132 20389059-10 2010 Thus, indoxyl sulfate may play an important role in the development of CVD in CKD by increasing the endothelial expression of ICAM-1 and MCP-1. Indican 6-21 C-C motif chemokine ligand 2 Homo sapiens 137-142 19494236-0 2009 ROS and PDGF-beta [corrected] receptors are critically involved in indoxyl sulfate actions that promote vascular smooth muscle cell proliferation and migration. Indican 67-82 platelet derived growth factor subunit B Homo sapiens 8-17 16825019-0 2006 Accumulation of indoxyl sulfate in OAT1/3-positive tubular cells in kidneys of patients with chronic renal failure. Indican 16-31 solute carrier family 22 member 6 Homo sapiens 35-39 18592293-2 2008 We have examined the underlying mechanism using, as a model system, glucose and indican (indoxyl-beta-D-glucopyranoside) transport by human Na+/glucose cotransporter (hSGLT1). Indican 80-87 solute carrier family 5 member 1 Homo sapiens 167-173 18592293-3 2008 Indican is transported by hSGLT1 at 10% of the rate for glucose but with a fivefold higher apparent affinity. Indican 0-7 solute carrier family 5 member 1 Homo sapiens 26-32 17403109-10 2007 In addition, the ROS production mediated by indoxyl sulfate was inhibited by the antioxidants vitamin C, vitamin E, and NAC. Indican 44-59 synuclein alpha Homo sapiens 120-123 17264878-0 2007 Indoxyl sulfate induces skeletal resistance to parathyroid hormone in cultured osteoblastic cells. Indican 0-15 parathyroid hormone Homo sapiens 47-66 17264878-8 2007 Furthermore, expression of organic anion transporter-3 (OAT-3) that is known to mediate cellular uptake of IS was identified in the primary osteoblast culture. Indican 107-109 solute carrier family 22 member 8 Homo sapiens 27-54 17264878-8 2007 Furthermore, expression of organic anion transporter-3 (OAT-3) that is known to mediate cellular uptake of IS was identified in the primary osteoblast culture. Indican 107-109 solute carrier family 22 member 8 Homo sapiens 56-61 19378798-1 2009 BACKGROUND: Oral adsorbent AST-120 reduces uremic toxins, such as indoxyl sulfate, and retards the progression of chronic kidney disease (CKD). Indican 66-81 solute carrier family 17 member 5 Homo sapiens 27-30 17207267-6 2007 Interestingly, of nine additionally tested plant cell suspension cultures from various plant families, five were also capable of the formation of indican after indole supplementation, although this metabolism was more pronounced in transgenic tobacco cell suspension cultures expressing CYP2A6 cDNA. Indican 146-153 cytochrome P450 family 2 subfamily A member 6 Homo sapiens 287-293 16825019-2 2006 Indoxyl sulfate is taken up by renal proximal tubular cells through organic anion transporters 1 and 3 (OAT1/3), and is accumulated in the renal proximal tubular cells of uremic rats. Indican 0-15 solute carrier family 22 member 6 Rattus norvegicus 68-102 16825019-2 2006 Indoxyl sulfate is taken up by renal proximal tubular cells through organic anion transporters 1 and 3 (OAT1/3), and is accumulated in the renal proximal tubular cells of uremic rats. Indican 0-15 solute carrier family 22 member 6 Rattus norvegicus 104-110 16825019-6 2006 Indoxyl sulfate was localized in the hOAT1- and hOAT3-positive renal tubular cells in the kidneys of CRF patients. Indican 0-15 solute carrier family 22 member 6 Homo sapiens 37-42 16825019-6 2006 Indoxyl sulfate was localized in the hOAT1- and hOAT3-positive renal tubular cells in the kidneys of CRF patients. Indican 0-15 solute carrier family 22 member 8 Homo sapiens 48-53 16825019-9 2006 In conclusion, in CRF patients, indoxyl sulfate is accumulated in the tubular cells with hOAT1 and/or hOAT3 localized at the basolateral membrane. Indican 32-47 solute carrier family 22 member 6 Homo sapiens 89-94 16825019-9 2006 In conclusion, in CRF patients, indoxyl sulfate is accumulated in the tubular cells with hOAT1 and/or hOAT3 localized at the basolateral membrane. Indican 32-47 solute carrier family 22 member 8 Homo sapiens 102-107 16564934-5 2006 RESULTS: AST-120 decreased serum indoxyl sulfate levels in a dose-dependent fashion. Indican 33-48 solute carrier family 17 member 5 Homo sapiens 9-12 15846470-11 2005 rOat1 and rOat3 contributed equally to the renal uptake of IS. Indican 59-61 solute carrier family 22 member 6 Rattus norvegicus 0-5 16085315-8 2006 Recent studies demonstrate that the uremic toxins CMPF and indoxyl sulfate (IS) can directly inhibit rOatp2 and hOATP-C in hepatocytes. Indican 59-74 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 101-107 16085315-8 2006 Recent studies demonstrate that the uremic toxins CMPF and indoxyl sulfate (IS) can directly inhibit rOatp2 and hOATP-C in hepatocytes. Indican 76-78 solute carrier organic anion transporter family, member 1a4 Rattus norvegicus 101-107 16405517-9 2006 In vitro, p-cresol and indoxyl sulfate significantly increased both CD146+ and annexin-V+ EMP release. Indican 23-38 melanoma cell adhesion molecule Homo sapiens 68-73 16405517-9 2006 In vitro, p-cresol and indoxyl sulfate significantly increased both CD146+ and annexin-V+ EMP release. Indican 23-38 annexin A5 Homo sapiens 79-88 15846470-11 2005 rOat1 and rOat3 contributed equally to the renal uptake of IS. Indican 59-61 solute carrier family 22 member 8 Rattus norvegicus 10-15 14675047-13 2004 Both OAT1 and OAT3 contribute almost equally to the renal uptake of IS. Indican 68-70 solute carrier family 22 member 6 Rattus norvegicus 5-9 14675047-13 2004 Both OAT1 and OAT3 contribute almost equally to the renal uptake of IS. Indican 68-70 solute carrier family 22 member 8 Rattus norvegicus 14-18 12675842-14 2003 Both antioxidant and NF-kappaB inhibitors dose dependently inhibited the activation of PAI-1 promoter by indoxyl sulfate. Indican 105-120 serpin family E member 1 Homo sapiens 87-92 12358729-0 2002 Role of blood-brain barrier organic anion transporter 3 (OAT3) in the efflux of indoxyl sulfate, a uremic toxin: its involvement in neurotransmitter metabolite clearance from the brain. Indican 80-95 solute carrier family 22 member 8 Rattus norvegicus 57-61 12675842-9 2003 RESULTS: Among organic anion species tested, indoxyl sulfate and indoleacetic acid induced free radical production in HK-2. Indican 45-60 hexokinase 2 Homo sapiens 118-122 12675842-11 2003 Indoxyl sulfate and indoleacetic acid dose dependently increased the expressions of PAI-1 mRNA and protein in these cells. Indican 0-15 serpin family E member 1 Homo sapiens 84-89 12675842-12 2003 The luciferase reporter gene assay revealed that indoxyl sulfate and indoleacetic acid dose dependently activated NF-kappaB and PAI-1 promoter. Indican 49-64 nuclear factor kappa B subunit 1 Homo sapiens 114-123 12675842-12 2003 The luciferase reporter gene assay revealed that indoxyl sulfate and indoleacetic acid dose dependently activated NF-kappaB and PAI-1 promoter. Indican 49-64 serpin family E member 1 Homo sapiens 128-133 12675842-14 2003 Both antioxidant and NF-kappaB inhibitors dose dependently inhibited the activation of PAI-1 promoter by indoxyl sulfate. Indican 105-120 nuclear factor kappa B subunit 1 Homo sapiens 21-30 12679137-6 2003 In conclusion, by comparing the K(i) values with the plasma concentration of unbound indoxyl sulfate, it was predicted that human-OAT1 and human-OAT3 mediate the transport of indoxyl sulfate in vivo. Indican 175-190 solute carrier family 22 member 8 Homo sapiens 145-149 12679137-7 2003 In addition, it was suggested that human-OAT1 and human-OAT3 are involved in the urinary excretion of indoxyl sulfate, the exacerbation of renal dysfunction and the induction of uremic encephalopathy by indoxyl sulfate. Indican 102-117 solute carrier family 22 member 6 Homo sapiens 41-45 12679137-7 2003 In addition, it was suggested that human-OAT1 and human-OAT3 are involved in the urinary excretion of indoxyl sulfate, the exacerbation of renal dysfunction and the induction of uremic encephalopathy by indoxyl sulfate. Indican 102-117 solute carrier family 22 member 8 Homo sapiens 56-60 12679137-7 2003 In addition, it was suggested that human-OAT1 and human-OAT3 are involved in the urinary excretion of indoxyl sulfate, the exacerbation of renal dysfunction and the induction of uremic encephalopathy by indoxyl sulfate. Indican 203-218 solute carrier family 22 member 6 Homo sapiens 41-45 12679137-7 2003 In addition, it was suggested that human-OAT1 and human-OAT3 are involved in the urinary excretion of indoxyl sulfate, the exacerbation of renal dysfunction and the induction of uremic encephalopathy by indoxyl sulfate. Indican 203-218 solute carrier family 22 member 8 Homo sapiens 56-60 12679720-4 2003 This elimination was significantly inhibited by para-aminohippuric acid (PAH), benzylpenicillin, indoxyl sulfate, and cimetidine, suggesting the involvement of rat organic anion transporter 3 (rOAT3). Indican 97-112 solute carrier family 22 member 8 Rattus norvegicus 193-198 12679720-5 2003 rOAT3-expressing oocytes exhibited [3H]HVA uptake (K(m) = 274 micromol/L), which was inhibited by several organic anions, such as PAH, indoxyl sulfate, octanoic acid, and metabolites of monoamine neurotransmitters. Indican 135-150 solute carrier family 22 member 8 Rattus norvegicus 0-5 12679137-3 2003 Indoxyl sulfate inhibited human-OAT1, human-OAT3 and human-OAT4, but not human-OAT2, human-OCT1 and human-OCT2. Indican 0-15 solute carrier family 22 member 6 Homo sapiens 32-36 12679137-3 2003 Indoxyl sulfate inhibited human-OAT1, human-OAT3 and human-OAT4, but not human-OAT2, human-OCT1 and human-OCT2. Indican 0-15 solute carrier family 22 member 8 Homo sapiens 44-48 12679137-3 2003 Indoxyl sulfate inhibited human-OAT1, human-OAT3 and human-OAT4, but not human-OAT2, human-OCT1 and human-OCT2. Indican 0-15 solute carrier family 22 member 11 Homo sapiens 59-63 12679137-5 2003 Human-OAT1 and human-OAT3 mediated the uptake of indoxyl sulfate and human-OAT4 mediated not only the uptake but also the efflux of indoxyl sulfate. Indican 49-64 solute carrier family 22 member 6 Homo sapiens 6-10 12679137-5 2003 Human-OAT1 and human-OAT3 mediated the uptake of indoxyl sulfate and human-OAT4 mediated not only the uptake but also the efflux of indoxyl sulfate. Indican 49-64 solute carrier family 22 member 8 Homo sapiens 21-25 12679137-5 2003 Human-OAT1 and human-OAT3 mediated the uptake of indoxyl sulfate and human-OAT4 mediated not only the uptake but also the efflux of indoxyl sulfate. Indican 132-147 solute carrier family 22 member 6 Homo sapiens 6-10 12679137-5 2003 Human-OAT1 and human-OAT3 mediated the uptake of indoxyl sulfate and human-OAT4 mediated not only the uptake but also the efflux of indoxyl sulfate. Indican 132-147 solute carrier family 22 member 8 Homo sapiens 21-25 12679137-5 2003 Human-OAT1 and human-OAT3 mediated the uptake of indoxyl sulfate and human-OAT4 mediated not only the uptake but also the efflux of indoxyl sulfate. Indican 132-147 solute carrier family 22 member 11 Homo sapiens 75-79 12679137-6 2003 In conclusion, by comparing the K(i) values with the plasma concentration of unbound indoxyl sulfate, it was predicted that human-OAT1 and human-OAT3 mediate the transport of indoxyl sulfate in vivo. Indican 85-100 solute carrier family 22 member 6 Homo sapiens 130-134 12679137-6 2003 In conclusion, by comparing the K(i) values with the plasma concentration of unbound indoxyl sulfate, it was predicted that human-OAT1 and human-OAT3 mediate the transport of indoxyl sulfate in vivo. Indican 85-100 solute carrier family 22 member 8 Homo sapiens 145-149 12679137-6 2003 In conclusion, by comparing the K(i) values with the plasma concentration of unbound indoxyl sulfate, it was predicted that human-OAT1 and human-OAT3 mediate the transport of indoxyl sulfate in vivo. Indican 175-190 solute carrier family 22 member 6 Homo sapiens 130-134 12358729-7 2002 These results suggest that OAT3 mediates the brain-to-blood transport of indoxyl sulfate, and is also involved in the efflux transport of neurotransmitter metabolites and drugs. Indican 73-88 solute carrier family 22 member 8 Rattus norvegicus 27-31 12089366-10 2002 These results suggest that rOAT1 and rOAT3 play an important role in the transcellular transport of IS and the induction of its nephrotoxicity. Indican 100-102 solute carrier family 22 member 6 Rattus norvegicus 27-32 12089366-10 2002 These results suggest that rOAT1 and rOAT3 play an important role in the transcellular transport of IS and the induction of its nephrotoxicity. Indican 100-102 solute carrier family 22 member 8 Rattus norvegicus 37-42 11867951-6 2002 In the CRF+BK group, the level of serum and urinary indoxyl sulfate and the tubular accumulation of indoxyl sulfate decreased. Indican 52-67 corticotropin releasing hormone Rattus norvegicus 7-19 11967025-0 2002 Major role of organic anion transporter 3 in the transport of indoxyl sulfate in the kidney. Indican 62-77 solute carrier family 22 member 8 Homo sapiens 14-41 11967025-10 2002 CONCLUSIONS: These results suggest that rOAT3 is responsible for the renal uptake of indoxyl sulfate, and uremic toxins share the transport mechanism for indoxyl sulfate. Indican 85-100 solute carrier family 22 member 8 Rattus norvegicus 40-45 11967025-10 2002 CONCLUSIONS: These results suggest that rOAT3 is responsible for the renal uptake of indoxyl sulfate, and uremic toxins share the transport mechanism for indoxyl sulfate. Indican 154-169 solute carrier family 22 member 8 Rattus norvegicus 40-45 12064372-1 2002 The aim of this study was to identify sulfotransferase (SULT) isoform(s) responsible for the formation of indoxyl sulfate from indoxyl (3-hydroxyindole). Indican 106-121 carbohydrate sulfotransferase 10 Rattus norvegicus 38-54 12064372-1 2002 The aim of this study was to identify sulfotransferase (SULT) isoform(s) responsible for the formation of indoxyl sulfate from indoxyl (3-hydroxyindole). Indican 106-121 carbohydrate sulfotransferase 10 Rattus norvegicus 56-60 12064372-5 2002 To help identify the isoform(s) of SULT responsible for indoxyl sulfate formation, indoxyl was incubated with human and rat liver cytosols and PAPS in the presence of isoform-specific SULT inhibitors. Indican 56-71 carbohydrate sulfotransferase 10 Rattus norvegicus 35-39 12064372-7 2002 However, an aryl (phenol) sulfotransferase inhibitor, 2,6-dichloro-4-nitrophenol (DCNP), inhibited the formation of indoxyl sulfate with a IC50 values of 3.2 microM for human and 1.0 microM for rat cytosol indicating that human and rat aryl (phenol) sulfotransferases are responsible for the formation of indoxyl sulfate. Indican 116-131 carbohydrate sulfotransferase 10 Rattus norvegicus 26-42 12064372-7 2002 However, an aryl (phenol) sulfotransferase inhibitor, 2,6-dichloro-4-nitrophenol (DCNP), inhibited the formation of indoxyl sulfate with a IC50 values of 3.2 microM for human and 1.0 microM for rat cytosol indicating that human and rat aryl (phenol) sulfotransferases are responsible for the formation of indoxyl sulfate. Indican 305-320 carbohydrate sulfotransferase 10 Rattus norvegicus 26-42 12064372-9 2002 Kinetic studies with human and rat cytosols and human recombinant SULT1A1*2 gave similar kinetic values indicating that human and rat aryl sulfotransferases efficiently catalyze the formation of indoxyl sulfate, an important uremic toxin metabolite. Indican 195-210 sulfotransferase family 1A member 1 Homo sapiens 66-73 11867951-6 2002 In the CRF+BK group, the level of serum and urinary indoxyl sulfate and the tubular accumulation of indoxyl sulfate decreased. Indican 100-115 corticotropin releasing hormone Rattus norvegicus 7-19 11815391-4 2002 Among the organic anions examined, hippuric acid, para-hydroxyhippuric acid, ortho-hydroxyhippuric acid, indoxyl sulphate and indoleacetic acid showed a high affinity for hOAT1 expressed in the OK cells. Indican 105-121 solute carrier family 22 member 6 Homo sapiens 171-176 11815391-5 2002 Indoxyl sulphate and indoleacetic acid concentration-dependently inhibited proliferation of the hOAT1-transformed cells. Indican 0-16 solute carrier family 22 member 6 Homo sapiens 96-101 11815391-11 2002 Less free radical production was observed in the hOAT1-transformed cells treated with p-hydroxyhippuric acid, o-hydroxyhippuric acid compared with indoxyl sulphate and indoleacetic acid. Indican 147-163 solute carrier family 22 member 6 Homo sapiens 49-54