PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26297582-15 2015 The impairment of the PI3K/AKT/eNOS pathway after physiological insulin treatment could contribute to detrimental effects on cardiovascular homeostasis under high glucose conditions, and might shift toward the activation of certain mitogenic effectors, such as ERK1/2, p38 and JNK, the only ones that respond to physiological insulin treatment in high glucose. Glucose 163-170 nitric oxide synthase 3 Homo sapiens 31-35 29702252-8 2018 The mechanism of inhibition of SGLT-1 was secondary to diminished affinity of the co-transporter for glucose in NOS3 silenced cells. Glucose 101-108 nitric oxide synthase 3 Homo sapiens 112-116 28565879-6 2017 Exposure of human umbilical vein endothelial cells (HUVEC) to a high glucose concentration decreased NO and endothelial nitric oxide synthase (eNOS) levels but increased inducible NOS (iNOS) levels. Glucose 69-76 nitric oxide synthase 3 Homo sapiens 108-141 26924495-7 2016 Fluctuating glucose, but not constant high glucose, significantly decreased the endothelial nitric oxide synthase (eNOS) phosphorylation level at Ser-1177 without affecting total eNOS expression, which was prevented by astaxanthin as well as by the anti-oxidant NAC. Glucose 12-19 nitric oxide synthase 3 Homo sapiens 80-113 26682233-7 2016 Additionally, Akt/eNOS activity and NO production were downregulated in high glucose-stimulated EPCs. Glucose 77-84 nitric oxide synthase 3 Homo sapiens 18-22 26682233-12 2016 CoQ10 reduced high glucose-induced EPC apoptosis and dysfunction through upregulation of eNOS, HO-1 through the AMPK pathway. Glucose 19-26 nitric oxide synthase 3 Homo sapiens 89-93 26297582-9 2015 RESULTS: In normal glucose, the active phosphorylated forms of AKT, eNOS, ERK1/2, p38 and JNK were increased in insulin treated cells, in a dose-dependent manner. Glucose 19-26 nitric oxide synthase 3 Homo sapiens 68-72 27583345-3 2016 Also in high glucose condition monomeric adiponectin increased eNOS and above kinases phosphorylation with similar patterns but at lower extent. Glucose 13-20 nitric oxide synthase 3 Homo sapiens 63-67 26385052-0 2015 Pharmacogenetic influence of eNOS gene variant on endothelial and glucose metabolism responses to L-arginine supplementation: Post hoc analysis of the L-arginine trial. Glucose 66-73 nitric oxide synthase 3 Homo sapiens 29-33 26297582-15 2015 The impairment of the PI3K/AKT/eNOS pathway after physiological insulin treatment could contribute to detrimental effects on cardiovascular homeostasis under high glucose conditions, and might shift toward the activation of certain mitogenic effectors, such as ERK1/2, p38 and JNK, the only ones that respond to physiological insulin treatment in high glucose. Glucose 352-359 nitric oxide synthase 3 Homo sapiens 31-35 25197782-5 2014 Moreover, high glucose reduced the levels of endothelial nitric oxide synthase (eNOS) phosphorylation, nitric oxide (NO) production and intracellular cyclic guanosine monophosphate (cGMP). Glucose 15-22 nitric oxide synthase 3 Homo sapiens 45-78 25938443-10 2015 In addition, P2X7 mediated both high glucose and palmitate-induced increase in reactive oxygen species levels and decrease in endothelial nitric oxide synthase. Glucose 37-44 nitric oxide synthase 3 Homo sapiens 126-159 24924461-8 2014 RESULTS: Comparing to the normal glucose group, high glucose treatment increased the cell damage, the level of NO and [Ca(2)+]i (P < 0.05) , downregulated CAMKIIdelta, eNOS expression and eNOS ser 1177 phosphorylation (P < 0.05), elevated the concentration of MDA and ROS (P < 0.05) in HUVECs. Glucose 53-60 nitric oxide synthase 3 Homo sapiens 171-175 24924461-8 2014 RESULTS: Comparing to the normal glucose group, high glucose treatment increased the cell damage, the level of NO and [Ca(2)+]i (P < 0.05) , downregulated CAMKIIdelta, eNOS expression and eNOS ser 1177 phosphorylation (P < 0.05), elevated the concentration of MDA and ROS (P < 0.05) in HUVECs. Glucose 53-60 nitric oxide synthase 3 Homo sapiens 191-195 23457308-0 2013 Ceramide mediates inhibition of the Akt/eNOS pathway by high levels of glucose in human vascular endothelial cells. Glucose 71-78 nitric oxide synthase 3 Homo sapiens 40-44 25016868-0 2014 [Effect of sequoyitol on expression of NOX4 and eNOS induced with glucose in human umbilical vein endothelial cells]. Glucose 66-73 nitric oxide synthase 3 Homo sapiens 48-52 23718875-1 2013 BACKGROUND: Our prior study revealed the loss in short-term L-Arginine (ARG) therapeutic efficacy after continuous exposure; resulting in tolerance development, mediated by endothelial nitric oxide synthase (eNOS) down-regulation, secondary to oxidative stress and induced glucose accumulation. Glucose 273-280 nitric oxide synthase 3 Homo sapiens 173-206 23457308-1 2013 OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs). Glucose 68-75 nitric oxide synthase 3 Homo sapiens 106-139 23457308-1 2013 OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs). Glucose 68-75 nitric oxide synthase 3 Homo sapiens 141-145 23457308-6 2013 We also show that exposure of HUVECs to high-glucose conditions inhibits the insulin-mediated activation of Akt/eNOS signalling and the subsequent NO generation in a dose-dependent manner (p<0.05). Glucose 45-52 nitric oxide synthase 3 Homo sapiens 112-116 23457308-7 2013 Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05). Glucose 82-89 nitric oxide synthase 3 Homo sapiens 108-112 22507035-11 2012 Western blot analysis revealed that high glucose downregulated the phosphorylation of AMPK and endothelial nitric oxide synthase, which could be reversed with TO treatment. Glucose 41-48 nitric oxide synthase 3 Homo sapiens 95-128 23063542-0 2012 Mechanism of reversal of high glucose-induced endothelial nitric oxide synthase uncoupling by tanshinone IIA in human endothelial cell line EA.hy926. Glucose 30-37 nitric oxide synthase 3 Homo sapiens 46-79 23457308-8 2013 CONCLUSION: Ceramide is both necessary and sufficient for mediating the inhibition of the Akt/eNOS signalling pathway by high-glucose levels in endothelial cells. Glucose 126-133 nitric oxide synthase 3 Homo sapiens 94-98 22207730-8 2012 Pharmacological AMP kinase activation led to phosphorylation of endothelial nitric oxide synthase"s Ser633 activation site, reversing the adverse effects of low glucose. Glucose 161-168 nitric oxide synthase 3 Homo sapiens 64-97 22518022-0 2012 Arginine attenuates methylglyoxal- and high glucose-induced endothelial dysfunction and oxidative stress by an endothelial nitric-oxide synthase-independent mechanism. Glucose 44-51 nitric oxide synthase 3 Homo sapiens 111-144 21747057-7 2011 Silencing Fis1 or Drp1 expression with siRNA blunted high glucose-induced alterations in mitochondrial networks, reactive oxygen species production, endothelial nitric oxide synthase activation, and cGMP production. Glucose 58-65 nitric oxide synthase 3 Homo sapiens 149-182 21844127-5 2011 Significant differences in glucose-induced cell death and free 3NT-induced cell death were observed among the NOS3 genotypes. Glucose 27-34 nitric oxide synthase 3 Homo sapiens 110-114 20448349-5 2010 The expression of PI3K, PKB, and eNOS in the intermittent high glucose group was significantly lower than that in the constant high glucose group (P<0.05). Glucose 63-70 nitric oxide synthase 3 Homo sapiens 33-37 20559724-1 2011 BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle. Glucose 220-227 nitric oxide synthase 3 Homo sapiens 76-109 20559724-1 2011 BACKGROUND: Nitric oxide (NO), synthesized from LS: -arginine by the enzyme endothelial nitric oxide synthase (eNOS), is a potent vasodilator and has been implicated in mediating insulin-induced uptake and metabolism of glucose in skeletal muscle. Glucose 220-227 nitric oxide synthase 3 Homo sapiens 111-115 21750782-8 2011 OxLDL, LDL and glucose decreased the eNOS protein level by 74 %, 37 % and 29 %, respectively. Glucose 15-22 nitric oxide synthase 3 Homo sapiens 37-41 20448349-5 2010 The expression of PI3K, PKB, and eNOS in the intermittent high glucose group was significantly lower than that in the constant high glucose group (P<0.05). Glucose 132-139 nitric oxide synthase 3 Homo sapiens 33-37 20448349-6 2010 CONCLUSION: Intermittent high glucose could be more deleterious to endothelial cells than constant high glucose, and may lead to decrease synthesis of NO by inhibiting PI3K/PKB/eNOS pathway activation. Glucose 30-37 nitric oxide synthase 3 Homo sapiens 177-181 18064606-1 2008 High D-glucose reduces human equilibrative nucleoside transporter 1 (hENT1)-mediated adenosine uptake involving endothelial nitric oxide synthase (eNOS), mitogen-activated protein (MAP) kinase kinases 1 and 2/MAP kinases p42/44 (MEK/ERKs), and protein kinase C (PKC) activation in human umbilical vein endothelium (HUVEC). Glucose 5-14 nitric oxide synthase 3 Homo sapiens 112-145 19878672-9 2010 Furthermore, high glucose attenuated eNOS protein and total nitrite levels. Glucose 18-25 nitric oxide synthase 3 Homo sapiens 37-41 19878672-11 2010 Collectively, our study demonstrates that high glucose-induced oxidative stress via NADPH oxidase activation and this contributed to LOX-1 upregulation and eNOS downregulation in human endothelial cells. Glucose 47-54 nitric oxide synthase 3 Homo sapiens 156-160 19767878-0 2009 Rosiglitazone inhibits high glucose-induced apoptosis in human umbilical vein endothelial cells through the PI3K/Akt/eNOS pathway. Glucose 28-35 nitric oxide synthase 3 Homo sapiens 117-121 19767878-1 2009 Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium. Glucose 161-168 nitric oxide synthase 3 Homo sapiens 75-108 19767878-1 2009 Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium. Glucose 161-168 nitric oxide synthase 3 Homo sapiens 124-128 19767878-4 2009 High glucose treatment also decreased Akt and eNOS phosphorylation levels with subsequent NO production. Glucose 5-12 nitric oxide synthase 3 Homo sapiens 46-50 19767878-8 2009 These findings suggest that rosiglitazone inhibits high glucose-induced apoptosis in HUVECs through the PI3K/Akt/eNOS pathway. Glucose 56-63 nitric oxide synthase 3 Homo sapiens 113-117 19229826-0 2009 Effect of glucose degradation products, glucose-containing dialysate and icodextrin on AQP1 and eNOS expression in cultured endothelial cells. Glucose 40-47 nitric oxide synthase 3 Homo sapiens 96-100 19229826-3 2009 We aimed at examining the effect of peritoneal dialysis solutions (PDSs) and glucose degradation products (GDPs) on the expression of AQP1 and eNOS in cultured endothelial cells. Glucose 77-84 nitric oxide synthase 3 Homo sapiens 143-147 19229826-7 2009 Glucose-based PDS as well as icodextrin PDS significantly up-regulated basal AQP1 and eNOS mRNA. Glucose 0-7 nitric oxide synthase 3 Homo sapiens 86-90 18841076-5 2008 Cytoprotective rLE substantially reduced high glucose-induced expression of endothelial nitric oxide synthase (eNOS), and hence attenuated the formation of peroxynitrite radicals derived from NO. Glucose 46-53 nitric oxide synthase 3 Homo sapiens 76-109 17427197-9 2007 High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. Glucose 5-14 nitric oxide synthase 3 Homo sapiens 50-54 18409050-8 2008 For the first time, results of our study suggest that crocetin inhibits high glucose-induced apoptosis, at least partly, via Pl3K/Akt/eNOS pathway in HUVECs and crocetin may exert a beneficial effect in preventing diabetes-associated cardiovascular complications. Glucose 77-84 nitric oxide synthase 3 Homo sapiens 134-138 18191076-4 2008 Constant high glucose levels increased p47-phox, p67-phox, and p22-phox expression [components of the Nicotinamide adenine dinucleotide phosphate [NAD(P)H] oxidase complex]; endothelial nitric oxide synthase, nitric oxide, and O(2)(-) production; nitrotyrosine, 8-hydroxy-2"-deoxyguanosine, and caspase-3 expression; and reduced Bcl-2 expression. Glucose 14-21 nitric oxide synthase 3 Homo sapiens 174-207 18409050-5 2008 High glucose attenuated activation of Akt and endothelial nitric oxide synthase (eNOS). Glucose 5-12 nitric oxide synthase 3 Homo sapiens 46-79 18409050-5 2008 High glucose attenuated activation of Akt and endothelial nitric oxide synthase (eNOS). Glucose 5-12 nitric oxide synthase 3 Homo sapiens 81-85 17716867-0 2007 Alpha-linolenic acid attenuates high glucose-induced apoptosis in cultured human umbilical vein endothelial cells via PI3K/Akt/eNOS pathway. Glucose 37-44 nitric oxide synthase 3 Homo sapiens 127-131 17716867-6 2007 Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose. Glucose 18-25 nitric oxide synthase 3 Homo sapiens 61-94 17716867-6 2007 Furthermore, high glucose reduced phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production, whereas ALA treatment attenuated the reduction caused by high glucose. Glucose 18-25 nitric oxide synthase 3 Homo sapiens 96-100 17716867-8 2007 CONCLUSION: ALA exerts an antiapoptotic effect by the phosphatidylinositol 3"-kinase/Akt/eNOS pathway in HUVECs exposed to high glucose and thus may represent a candidate therapeutic agent for diabetic cardiovascular complications. Glucose 128-135 nitric oxide synthase 3 Homo sapiens 89-93 17427197-6 2007 TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. Glucose 19-28 nitric oxide synthase 3 Homo sapiens 231-235 17427197-6 2007 TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. Glucose 19-28 nitric oxide synthase 3 Homo sapiens 274-278 16123371-0 2005 Variation in the eNOS gene modifies the association between total energy expenditure and glucose intolerance. Glucose 89-96 nitric oxide synthase 3 Homo sapiens 17-21 17082313-0 2007 17beta-estradiol antagonizes the down-regulation of endothelial nitric-oxide synthase and GTP cyclohydrolase I by high glucose: relevance to postmenopausal diabetic cardiovascular disease. Glucose 119-126 nitric oxide synthase 3 Homo sapiens 52-85 17082313-8 2007 Transfection of small-interfering RNA targeting eNOS resulted in a marked reduction in GTPCH-I mRNA under both normal and high-glucose conditions, but this reduction was strongly reversed by 17beta-E2. Glucose 127-134 nitric oxide synthase 3 Homo sapiens 48-52 15970429-0 2006 High glucose-induced apoptosis in human vascular endothelial cells is mediated through NF-kappaB and c-Jun NH2-terminal kinase pathway and prevented by PI3K/Akt/eNOS pathway. Glucose 5-12 nitric oxide synthase 3 Homo sapiens 161-165 15970429-3 2006 The results showed that high glucose-induced apoptosis was significantly enhanced by PI3K inhibitors (wortmannin and LY294002), NOS inhibitor (NG-nitro-arginine methyl ester) and eNOS antisense oligonucleotide. Glucose 29-36 nitric oxide synthase 3 Homo sapiens 179-183 15970429-6 2006 Moreover, high glucose-induced increase in eNOS expression was attenuated by PI3K inhibitors and the negative mutant of PI3K. Glucose 15-22 nitric oxide synthase 3 Homo sapiens 43-47 15970429-9 2006 Activation of the ROS/PI3K/Akt/eNOS signaling pathway in early phase exerts protective effects against the induction of apoptosis by high glucose. Glucose 138-145 nitric oxide synthase 3 Homo sapiens 31-35 16472125-6 2006 Data obtained in the present study show that the exposure for 5 days to high glucose increases oxidative stress, reduces DDAH-2 and eNOS expression and increases iNOS expression. Glucose 77-84 nitric oxide synthase 3 Homo sapiens 132-136 16472125-7 2006 These results indicate that DDAH-2 and iNOS/eNOS dysregulation may play a key role in high glucose-mediated oxidative stress, suggesting that selective modulation of DDAH isoforms may result in selective inhibition/activation of NOS isoforms, thereby providing a novel strategy of approach in vascular complications of several pathologies. Glucose 91-98 nitric oxide synthase 3 Homo sapiens 44-48 16022682-2 2005 The aim of the present study was to determine the relative contributions of glucose and AGE (advanced glycation end-product) accumulation in suppressing NOS-3 (the endothelial isoform of NO synthase). Glucose 76-83 nitric oxide synthase 3 Homo sapiens 153-158 17082313-9 2007 These results suggest that the activation of ERalpha with 17beta-E2 can counteract high-glucose-induced down-regulation of eNOS and GTPCH-I in endothelial cells. Glucose 88-95 nitric oxide synthase 3 Homo sapiens 123-127 16443786-6 2006 Finally, incubation of BAECs with clinically relevant concentrations of metformin dramatically attenuated high-glucose (30 mmol/l)-induced reduction in the association of hsp90 with eNOS, which resulted in increased NO bioactivity with a reduction in overexpression of adhesion molecules and endothelial apoptosis caused by high-glucose exposure. Glucose 111-118 nitric oxide synthase 3 Homo sapiens 182-186 16443786-6 2006 Finally, incubation of BAECs with clinically relevant concentrations of metformin dramatically attenuated high-glucose (30 mmol/l)-induced reduction in the association of hsp90 with eNOS, which resulted in increased NO bioactivity with a reduction in overexpression of adhesion molecules and endothelial apoptosis caused by high-glucose exposure. Glucose 329-336 nitric oxide synthase 3 Homo sapiens 182-186 16123371-2 2005 Energy expenditure induces the endothelial NO synthase (eNOS) gene, providing a mechanism for insulin-independent glucose disposal. Glucose 114-121 nitric oxide synthase 3 Homo sapiens 31-54 16123371-2 2005 Energy expenditure induces the endothelial NO synthase (eNOS) gene, providing a mechanism for insulin-independent glucose disposal. Glucose 114-121 nitric oxide synthase 3 Homo sapiens 56-60 16123371-9 2005 Genetic variation at the eNOS locus is associated with diabetes, which may be attributable to an enhanced effect of total energy expenditure on glucose disposal in individuals with specific eNOS haplotypes. Glucose 144-151 nitric oxide synthase 3 Homo sapiens 25-29 16123371-9 2005 Genetic variation at the eNOS locus is associated with diabetes, which may be attributable to an enhanced effect of total energy expenditure on glucose disposal in individuals with specific eNOS haplotypes. Glucose 144-151 nitric oxide synthase 3 Homo sapiens 190-194 15526284-0 2005 Up-regulation of the association between heat shock protein 90 and endothelial nitric oxide synthase prevents high glucose-induced apoptosis in human endothelial cells. Glucose 115-122 nitric oxide synthase 3 Homo sapiens 67-100 15526284-3 2005 High glucose can trigger endothelial cell apoptosis by de-activation of endothelial nitric oxide synthase (eNOS). Glucose 5-12 nitric oxide synthase 3 Homo sapiens 72-105 15526284-3 2005 High glucose can trigger endothelial cell apoptosis by de-activation of endothelial nitric oxide synthase (eNOS). Glucose 5-12 nitric oxide synthase 3 Homo sapiens 107-111 15526284-5 2005 Yet, little is known about the molecular mechanisms that regulate eNOS activity during high glucose exposure. Glucose 92-99 nitric oxide synthase 3 Homo sapiens 66-70 15526284-6 2005 The present study was designed to determine the involvement of protein interactions between eNOS and HSP90 in high glucose-induced endothelial cell apoptosis. Glucose 115-122 nitric oxide synthase 3 Homo sapiens 92-96 15526284-8 2005 The results showed that the protein interactions between eNOS and HSP90 and between eNOS and Akt and the phosphorylation of eNOS were up-regulated by high glucose exposure for 2-4 h. With longer exposures, these effects decreased gradually. Glucose 155-162 nitric oxide synthase 3 Homo sapiens 57-61 15526284-8 2005 The results showed that the protein interactions between eNOS and HSP90 and between eNOS and Akt and the phosphorylation of eNOS were up-regulated by high glucose exposure for 2-4 h. With longer exposures, these effects decreased gradually. Glucose 155-162 nitric oxide synthase 3 Homo sapiens 84-88 15526284-8 2005 The results showed that the protein interactions between eNOS and HSP90 and between eNOS and Akt and the phosphorylation of eNOS were up-regulated by high glucose exposure for 2-4 h. With longer exposures, these effects decreased gradually. Glucose 155-162 nitric oxide synthase 3 Homo sapiens 84-88 15526284-12 2005 From our results we propose that, in HUVECs, during early phase of high glucose exposure, apoptosis can be prevented by enhancement of eNOS activity through augmentation of the protein interaction between eNOS and HSP90 and recruitment of the activated Akt. Glucose 72-79 nitric oxide synthase 3 Homo sapiens 135-139 15526284-12 2005 From our results we propose that, in HUVECs, during early phase of high glucose exposure, apoptosis can be prevented by enhancement of eNOS activity through augmentation of the protein interaction between eNOS and HSP90 and recruitment of the activated Akt. Glucose 72-79 nitric oxide synthase 3 Homo sapiens 205-209 15526284-14 2005 The present study provides a molecular basis for the effects of eNOS in the prevention of endothelial cells apoptosis during early phase of high glucose exposure. Glucose 145-152 nitric oxide synthase 3 Homo sapiens 64-68 15490108-3 2004 The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose. Glucose 139-146 nitric oxide synthase 3 Homo sapiens 59-92 15490108-3 2004 The aim of this study was to investigate the regulation of endothelial nitric oxide synthase (eNOS) activity by acute and chronic elevated glucose. Glucose 139-146 nitric oxide synthase 3 Homo sapiens 94-98 15490108-8 2004 RESULTS: Acute exposure (4 h) of human aortic endothelial cells to 25 mmol/l glucose moderately increased eNOS activity and eNOS mRNA and protein expression. Glucose 77-84 nitric oxide synthase 3 Homo sapiens 106-110 15490108-8 2004 RESULTS: Acute exposure (4 h) of human aortic endothelial cells to 25 mmol/l glucose moderately increased eNOS activity and eNOS mRNA and protein expression. Glucose 77-84 nitric oxide synthase 3 Homo sapiens 124-128 15490108-9 2004 In contrast, chronic exposure to elevated glucose (25 mmol/l for 7 days) reduced total nitrite levels (46% reduction), levels of eNOS mRNA (46% reduction) and eNOS protein (65% reduction). Glucose 42-49 nitric oxide synthase 3 Homo sapiens 129-133 15351621-10 2004 RESULTS: The least expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in HCSMCs was observed in cells exposed to 27 mM glucose alone. Glucose 130-137 nitric oxide synthase 3 Homo sapiens 33-48 15140758-9 2004 We concluded that eNOS in the renal glomerular capillary endothelial cells is suppressed by activity of PKC at high-glucose concentrations comparable to those in diabetic animals and humans. Glucose 116-123 nitric oxide synthase 3 Homo sapiens 18-22 15351621-10 2004 RESULTS: The least expression of endothelial NOS (eNOS) and inducible NOS (iNOS) in HCSMCs was observed in cells exposed to 27 mM glucose alone. Glucose 130-137 nitric oxide synthase 3 Homo sapiens 50-54 11118505-7 2000 D-Glucose and PMA increased endothelial NOS (eNOS) activity, which was prevented by calphostin C or omission of extracellular Ca2+ and unaffected by PD-98059. Glucose 0-9 nitric oxide synthase 3 Homo sapiens 28-43 12824263-0 2003 High glucose-induced tyrosine nitration in endothelial cells: role of eNOS uncoupling and aldose reductase activation. Glucose 5-12 nitric oxide synthase 3 Homo sapiens 70-74 12824263-7 2003 RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS). Glucose 37-44 nitric oxide synthase 3 Homo sapiens 203-236 12824263-7 2003 RESULTS: Increased concentrations of glucose or 3-methyL-o-glucose stimulated formation of nitric oxide (NO) and superoxide induced protein nitration on tyrosine and increased expression and activity of endothelial nitric oxide synthase (eNOS). Glucose 37-44 nitric oxide synthase 3 Homo sapiens 238-242 12824263-9 2003 CONCLUSIONS: Increases in glucose levels and osmotic stress similar to those in diabetic patients increase the formation of nitrotyrosine in retinal endothelial cells because of their actions increasing NOS activity and causing superoxide formation due to eNOS uncoupling and AR activation. Glucose 26-33 nitric oxide synthase 3 Homo sapiens 256-260 11562476-6 2001 Nitric oxide also found to have a profound effect in cell metabolism, because ECV304+eNOS cells had lower steady state levels of ATP and higher utilization of glucose via the glycolytic pathway than ECV304 cells. Glucose 159-166 nitric oxide synthase 3 Homo sapiens 85-89 15490108-9 2004 In contrast, chronic exposure to elevated glucose (25 mmol/l for 7 days) reduced total nitrite levels (46% reduction), levels of eNOS mRNA (46% reduction) and eNOS protein (65% reduction). Glucose 42-49 nitric oxide synthase 3 Homo sapiens 159-163 15490108-14 2004 CONCLUSIONS/INTERPRETATION: In diabetes, the expression and activity of eNOS is regulated through glucose-mediated mitochondrial production of reactive oxygen species and activation of the oxidative stress transcription factor AP-1. Glucose 98-105 nitric oxide synthase 3 Homo sapiens 72-76 14610325-5 2003 In addition, we evaluated the effect of glucose on the expression of endothelial nitric oxide synthase (eNOS) in HGECs by Western blotting. Glucose 40-47 nitric oxide synthase 3 Homo sapiens 69-102 14610325-5 2003 In addition, we evaluated the effect of glucose on the expression of endothelial nitric oxide synthase (eNOS) in HGECs by Western blotting. Glucose 40-47 nitric oxide synthase 3 Homo sapiens 104-108 14610325-7 2003 However, Western blot analysis revealed that eNOS protein expression was significantly upregulated at 12 h after exposure to high glucose concentrations (30 mM), reaching a peak at 48 h (twofold increase over baseline levels). Glucose 130-137 nitric oxide synthase 3 Homo sapiens 45-49 14610325-10 2003 CONCLUSIONS: The present study demonstrated that high glucose increased eNOS protein expression, but decreased NO release finally. Glucose 54-61 nitric oxide synthase 3 Homo sapiens 72-76 12055099-7 2002 The data strongly suggest, but do not definitely prove, that glucose indeed has the ability to stimulate both cNOS and iNOS in the islets and that NO might serve as a negative feedback inhibitor of glucose-stimulated insulin release. Glucose 61-68 nitric oxide synthase 3 Homo sapiens 110-114 11181410-3 2001 Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187. Glucose 70-77 nitric oxide synthase 3 Homo sapiens 184-217 11181410-3 2001 Here we demonstrate that acute exposure of human endothelial cells to glucose, at levels found in plasma of diabetic patients, results in a significant blunting of NO responses to the endothelial nitric oxide synthase (eNOS) agonists bradykinin and A-23187. Glucose 70-77 nitric oxide synthase 3 Homo sapiens 219-223 9236411-10 1997 CONCLUSIONS: The present study demonstrates that prolonged exposure to high glucose increases eNOS gene expression, protein expression, and NO release. Glucose 76-83 nitric oxide synthase 3 Homo sapiens 94-98 11593517-1 1999 OBJECTIVE: To observe the effects of nerve growth factor (NGF) on nitric oxide (NO) release and constitutive nitric oxide synthase (cNOS) gene expression in oxygen/glucose deprived cortical neuron cultures. Glucose 164-171 nitric oxide synthase 3 Homo sapiens 132-136 8532063-13 1995 Expression is enhanced by e.g. estrogens (for NOS I and III), shear stress, TGF-beta 1, and (in certain endothelial cells) high glucose (for NOS III). Glucose 128-135 nitric oxide synthase 3 Homo sapiens 141-148 31269778-5 2019 High glucose concentrations lead to a loss of mitochondrial networks, increased reactive oxygen species (ROS), endothelial nitric oxide synthase (eNOS) activation and a reduction in cGMP production related to protein kinase G (PKG) activity. Glucose 5-12 nitric oxide synthase 3 Homo sapiens 146-150 34218226-5 2021 In addition, we found that TSG not only increased the expression of Bcl-2, while decreasing Bax expression, but also activated phosphorylation of Akt and endothelial nitric oxide synthase (eNOS) with subsequent nitric oxide production and ultimately reduced high glucose-induced apoptosis. Glucose 263-270 nitric oxide synthase 3 Homo sapiens 154-187 35441585-6 2022 Cabozantinib ameliorated high glucose-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO) in hGECs. Glucose 30-37 nitric oxide synthase 3 Homo sapiens 77-110 35441585-6 2022 Cabozantinib ameliorated high glucose-induced reduction in the expression of endothelial nitric oxide synthase (eNOS) and the production of nitric oxide (NO) in hGECs. Glucose 30-37 nitric oxide synthase 3 Homo sapiens 112-116 32508185-6 2020 In endothelial cells from patients with T2DM, normal glucose conditions (24 hours at 5 mmol/L) lowered O-GlcNAc levels and restored insulin-mediated activation of endothelial nitric oxide synthase, whereas high glucose conditions (30 mmol/L) maintained both O-GlcNAc levels and impaired insulin action. Glucose 53-60 nitric oxide synthase 3 Homo sapiens 163-196 32508185-7 2020 Treatment of endothelial cells with Thiamet G, an O-GlcNAcase inhibitor, increased O-GlcNAc levels and blunted the improvement of insulin-mediated endothelial nitric oxide synthase phosphorylation by glucose normalization. Glucose 200-207 nitric oxide synthase 3 Homo sapiens 147-180 32508185-8 2020 Conclusions Taken together, our findings indicate a role for O-GlcNAc modification in the dynamic, glucose-induced impairment of endothelial nitric oxide synthase activation in endothelial cells from patients with T2DM. Glucose 99-106 nitric oxide synthase 3 Homo sapiens 129-162 34953892-9 2022 Western blotting showed a higher level of SREBP2, iNOS, and VEGF and a lower eNOS level in the higher glucose groups. Glucose 102-109 nitric oxide synthase 3 Homo sapiens 77-81 34605247-1 2021 Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production. Glucose 47-54 nitric oxide synthase 3 Homo sapiens 80-113 34605247-1 2021 Rationale: In diabetic animals as well as high glucose cell culture conditions, endothelial nitric oxide synthase (eNOS) is heavily O-GlcNAcylated, which inhibits its phosphorylation and nitric oxide (NO) production. Glucose 47-54 nitric oxide synthase 3 Homo sapiens 115-119 34605247-8 2021 Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production. Glucose 39-46 nitric oxide synthase 3 Homo sapiens 111-115 34605247-8 2021 Inhibition of glycolysis via 2-deoxy-2-glucose (2-DG) in cells exposed to disturbed flow efficiently decreased eNOS O-GlcNAcylation, thereby increasing eNOS phosphorylation and NO production. Glucose 39-46 nitric oxide synthase 3 Homo sapiens 152-156 34050207-2 2021 Previous studies found that Thr866 is the key site for low-glucose-mediated regulation of eNOS O-GlcNAc. Glucose 59-66 nitric oxide synthase 3 Homo sapiens 90-94 33967958-7 2021 Results: High (>16.7 mmol/L) concentration of glucose upregulated the expression of miR-21, leading to the activation and inhibition of the PTEN/AKT/eNOS and MAPK/ET-1 pathways, and upregulation of NO and downregulation of ET-1 secretion, respectively. Glucose 46-53 nitric oxide synthase 3 Homo sapiens 149-153 32103904-0 2020 Hydrogen Sulfide Protects Against High Glucose-Induced Human Umbilical Vein Endothelial Cell Injury Through Activating PI3K/Akt/eNOS Pathway. Glucose 39-46 nitric oxide synthase 3 Homo sapiens 128-132 31269778-5 2019 High glucose concentrations lead to a loss of mitochondrial networks, increased reactive oxygen species (ROS), endothelial nitric oxide synthase (eNOS) activation and a reduction in cGMP production related to protein kinase G (PKG) activity. Glucose 5-12 nitric oxide synthase 3 Homo sapiens 111-144