PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 33945148-0 2021 Dexmedetomidine targets miR-146a and participates in the progress of chronic obstructive pulmonary disease in vivo and in vitro. Dexmedetomidine 0-15 microRNA 146a Homo sapiens 24-32 33945148-10 2021 Additionally, dexmedetomidine was showed to reduce the 16HBEL cell apoptosis through reducing the expression of miR-146a. Dexmedetomidine 14-29 microRNA 146a Homo sapiens 112-120 33945148-11 2021 Moreover, dexmedetomidine regulated cell apoptosis and cell apoptosis through miR-146a in AEC2 cells. Dexmedetomidine 10-25 microRNA 146a Homo sapiens 78-86 33945148-13 2021 CONCLUSION: Dexmedetomidine reduced 16HBE cells and AEC2 cell apoptosis and attenuated COPD by down-regulating miR-146a. Dexmedetomidine 12-27 microRNA 146a Homo sapiens 111-119 25646371-0 2015 Role of miR-146a in regulation of the acute inflammatory response to monosodium urate crystals. Uric Acid 69-85 microRNA 146a Homo sapiens 8-16 33975513-6 2021 Three miRNAs (miR-146a-5p, miR-122-5p and miR-21-5p) were identified using expression pattern analysis, and the levels were significantly decreased after acitretin treatment (P< 0.001). Acitretin 154-163 microRNA 146a Homo sapiens 14-22 34716993-2 2022 The present study aimed to investigate the regulatory mechanism employed by miR-146a to control Tregs differentiation and function in AR. tregs 96-101 microRNA 146a Homo sapiens 76-84 34716993-8 2022 There were significantly fewer Tregs in miR-146a knockdown or STAT5b knockdown PBMCs compared to control PBMCs. tregs 31-36 microRNA 146a Homo sapiens 40-48 34716993-12 2022 CONCLUSIONS: miR-146a enhances Tregs differentiation and function in AR by positively targeting STAT5b. tregs 31-36 microRNA 146a Homo sapiens 13-21 34968770-6 2022 Our results showed that HBV infection significantly enhanced the levels of m6A modification and elevated the expression of METTL3 and mature-miR-146a-5p in THLE-2 cells, which was repressed by cycloleucine (m6A inhibitor). Cycloleucine 193-205 microRNA 146a Homo sapiens 141-149 34002665-4 2021 MiR-146a-5p up-regulation ameliorated the inflammatory reaction and cell barrier damage of HSAECs induced by PAF, and inhibited the apoptosis; besides, miR-146a-5p down-regulation functioned oppositely. Platelet Activating Factor 109-112 microRNA 146a Homo sapiens 0-8 34315248-6 2021 The apoptosis and autophagy, and related proteins were detected in chondrocytes treated with miR-146a-5p mimic/inhibitor or pcDNA3.1-NUMB/si-NUMB and IL-1beta, respectively. CHEMBL3740941 102-104 microRNA 146a Homo sapiens 93-101 34838994-4 2022 Free radical scavenging cerium oxide nanoparticles (CNP) conjugated to the anti-inflammatory microRNA-146a (miR146a), termed CNP-miR146a, have been shown to prevent acute lung injury in a pre-clinical model. ceric oxide 24-36 microRNA 146a Homo sapiens 93-106 34838994-4 2022 Free radical scavenging cerium oxide nanoparticles (CNP) conjugated to the anti-inflammatory microRNA-146a (miR146a), termed CNP-miR146a, have been shown to prevent acute lung injury in a pre-clinical model. ceric oxide 24-36 microRNA 146a Homo sapiens 108-115 34877498-5 2021 In septic patients, the plasma miR-146a-5p concentrations are closely associated with the two sepsis outcome predictors, blood lactate and coagulopathy. Lactic Acid 127-134 microRNA 146a Homo sapiens 31-39 34758885-7 2021 In addition, METH down-regulated the expression of the HIV restriction microRNAs (miR-28, miR-29a, miR-125b, miR-146a, miR-155, miR-223, and miR-382). Methamphetamine 13-17 microRNA 146a Homo sapiens 109-117 34656164-6 2021 Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells" renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells. Erlotinib Hydrochloride 162-171 microRNA 146a Homo sapiens 53-61 34748956-0 2022 Cerium oxide nanoparticle conjugation to microRNA-146a mechanism of correction for impaired diabetic wound healing. ceric oxide 0-12 microRNA 146a Homo sapiens 41-54 34748956-2 2022 We have shown that CNP-miR146a synthesized by the conjugation of cerium oxide nanoparticles (CNP) to microRNA (miR)-146a, improves diabetic wound healing. ceric oxide 65-77 microRNA 146a Homo sapiens 23-30 34748956-2 2022 We have shown that CNP-miR146a synthesized by the conjugation of cerium oxide nanoparticles (CNP) to microRNA (miR)-146a, improves diabetic wound healing. ceric oxide 65-77 microRNA 146a Homo sapiens 101-120 34748956-3 2022 CNP are divalent metal oxides that act as free radical scavenger, while miR146a inhibits the pro-inflammatory NFkappaB pathway, so CNP-miR146a has a synergistic role in modulating both oxidative stress and inflammation. metal oxides 17-29 microRNA 146a Homo sapiens 135-142 34796180-13 2021 In particular, we demonstrated that HLSC-EVs shuttled miR-146a-5p and that treatment with HLSC-EVs increased miR-146a-5p expression in LX-2. hlsc-evs 36-44 microRNA 146a Homo sapiens 54-62 34796180-13 2021 In particular, we demonstrated that HLSC-EVs shuttled miR-146a-5p and that treatment with HLSC-EVs increased miR-146a-5p expression in LX-2. hlsc-evs 36-44 microRNA 146a Homo sapiens 109-117 34796180-13 2021 In particular, we demonstrated that HLSC-EVs shuttled miR-146a-5p and that treatment with HLSC-EVs increased miR-146a-5p expression in LX-2. hlsc-evs 90-98 microRNA 146a Homo sapiens 109-117 34837916-5 2021 RESULTS: miR146a genotypes revealed that there was significant association between TT and TC genotypes with MF. Technetium 90-92 microRNA 146a Homo sapiens 9-16 34656164-6 2021 Functionally, the sponge type of TUSC7 regulation of miR-146a inhibited Notch signaling functions, and affected the cancer progression and stem cells" renewal in Erlotinib resistant PC9 cells (PC9ER) and Erlotinib resistant HCC827 cells (HCC827ER) cells. Erlotinib Hydrochloride 204-213 microRNA 146a Homo sapiens 53-61 34722233-0 2021 CircFAM114A2 Promotes Cisplatin Sensitivity via miR-222-3p/P27 and miR-146a-5p/P21 Cascades in Urothelial Carcinoma. Cisplatin 22-31 microRNA 146a Homo sapiens 67-75 34503396-11 2022 It is possible that miR-146a may be associated with vitamin D deficiency and disease disability, while miR-155 may be associated with the number of attacks. Vitamin D 52-61 microRNA 146a Homo sapiens 20-28 34334202-0 2021 The human milk oligosaccharide 2"-fucosyllactose attenuates beta-lactoglobulin-induced food allergy through the miR-146a-mediated toll-like receptor 4/nuclear factor-kappaB signaling pathway. Oligosaccharides 15-30 microRNA 146a Homo sapiens 112-120 34334202-0 2021 The human milk oligosaccharide 2"-fucosyllactose attenuates beta-lactoglobulin-induced food allergy through the miR-146a-mediated toll-like receptor 4/nuclear factor-kappaB signaling pathway. 2'-fucosyllactose 31-48 microRNA 146a Homo sapiens 112-120 34604205-4 2021 Both prostaglandin E1 and cyclooxygenase 2 (COX2) expression were the highest in the MALAT1 HYPO + miR-146a HYPER group and the lowest in the MALAT1 HYPER + miR-146a HYPO group. Alprostadil 5-21 microRNA 146a Homo sapiens 99-107 34243103-6 2021 Circulating miR-125a-5p (p=0.001), miR-146a-5p (p<0.001), and miR-155 (p=0.013) were reduced after 4-month treatment with DMF. Dimethyl Fumarate 122-125 microRNA 146a Homo sapiens 35-43 34246297-9 2021 Five of those miRNAs (hsa-miR-126-3p, hsa-miR-142-3p, hsa-miR-146a-5p, hsa-miR-155-5p, and hsa-miR-222-3p) also had a positive correlation with serum creatinine and therefore a negative correlation with eGFR. Creatinine 150-160 microRNA 146a Homo sapiens 54-66 34603024-11 2021 Conclusion: Our research demonstrated the potential of using ANRIL rs1333049 (G > C) and miR-146A rs2910164 (C > G) as biomarkers to support the prediction of a better prognosis for lung cancer patients receiving platinum-based chemotherapy. Platinum 213-221 microRNA 146a Homo sapiens 89-97 34141159-7 2021 Spirulina platensis administration exhibited a nephroprotective impact on R, TAA, and R/TAA toxicities via regulating miR-1 and miR-146a mRNA gene expression that monitored adenosine monophosphate-activated protein kinase/mammalian target of rapamycin signaling. Adenosine 173-182 microRNA 146a Homo sapiens 128-136 35129780-0 2022 MALAT-1/p53/miR-155/miR-146a ceRNA circuit tuned by methoxylated quercitin glycoside alters immunogenic and oncogenic profiles of breast cancer. quercitin glycoside 65-84 microRNA 146a Homo sapiens 20-28 35588772-7 2022 Based on weighted quantile sum (WQS) regression, we found positive associations of phthalate metabolites mixture with miR-146a, miR-125 b, and miR-222, and individual MMP and MBP were the major contributors. phthalic acid 83-92 microRNA 146a Homo sapiens 118-126 35588772-10 2022 Our findings suggested that certain phthalates exposure was related to plasma miRNAs alterations in a dose-response manner and miR-146a might partly mediate phthalate-associated ABI reduction. phthalic acid 157-166 microRNA 146a Homo sapiens 127-135 35444657-5 2022 However, miR146a was significantly decreased in SLE patients compared to healthy controls and was negatively correlated with plasma estradiol levels and with SLE disease activity scores (SLEDAI). Estradiol 132-141 microRNA 146a Homo sapiens 9-16 35241643-6 2022 Additionally, miR-146a overexpression weakened the metformin-mediated upregulation of NAMPT expression, NAD+ synthesis, SIRT activity, and senescence protection, whereas treatment with the miR-146a inhibitor reversed this effect. Metformin 51-60 microRNA 146a Homo sapiens 189-197 35241643-6 2022 Additionally, miR-146a overexpression weakened the metformin-mediated upregulation of NAMPT expression, NAD+ synthesis, SIRT activity, and senescence protection, whereas treatment with the miR-146a inhibitor reversed this effect. NAD 104-108 microRNA 146a Homo sapiens 14-22 35241643-9 2022 AMPK activators metformin and 5-aminoimidazole-4-carboxamide (AICAR) hindered miR-146a expression at the transcriptional level by promoting IkappaB kinase (IKK) phosphorylation to attenuate nuclear factor-kappaB (NF-kappaB) activity. Metformin 16-25 microRNA 146a Homo sapiens 78-86 35241643-9 2022 AMPK activators metformin and 5-aminoimidazole-4-carboxamide (AICAR) hindered miR-146a expression at the transcriptional level by promoting IkappaB kinase (IKK) phosphorylation to attenuate nuclear factor-kappaB (NF-kappaB) activity. Aminoimidazole Carboxamide 30-60 microRNA 146a Homo sapiens 78-86 35241643-9 2022 AMPK activators metformin and 5-aminoimidazole-4-carboxamide (AICAR) hindered miR-146a expression at the transcriptional level by promoting IkappaB kinase (IKK) phosphorylation to attenuate nuclear factor-kappaB (NF-kappaB) activity. acadesine 62-67 microRNA 146a Homo sapiens 78-86 35241643-10 2022 These findings identified a novel cascade that negatively regulates the NAD+/SIRT pathway by suppressing miR-146a-mediated NAMPT downregulation. NAD 72-76 microRNA 146a Homo sapiens 105-113 35241643-12 2022 This mutual inhibitory relationship between miR-146a and AMPK enriches our understanding of the molecular connections between AMPK and SIRT and provides new insight into miRNA-mediated NAD+/SIRT regulation and an intervention point for the prevention of aging and age-related diseases. NAD 185-189 microRNA 146a Homo sapiens 44-52 34052997-7 2021 BMSCs-exosomal miR-146a-5p silencing promoted the proportions of Th17 cells and repressed the proportions of Tregs in CD4+ T cells. tregs 109-114 microRNA 146a Homo sapiens 15-23 35241643-0 2022 miR-146a impedes the anti-aging effect of AMPK via NAMPT suppression and NAD+/SIRT inactivation. NAD 73-77 microRNA 146a Homo sapiens 0-8 35241643-6 2022 Additionally, miR-146a overexpression weakened the metformin-mediated upregulation of NAMPT expression, NAD+ synthesis, SIRT activity, and senescence protection, whereas treatment with the miR-146a inhibitor reversed this effect. Metformin 51-60 microRNA 146a Homo sapiens 14-22 35222878-4 2022 Overexpression of miR-146a obviously reduced cell proliferation and tumorigenesis in vitro, as determined by MTT analysis, colony formation analysis, EdU analysis, and cell cycle experiments. monooxyethylene trimethylolpropane tristearate 109-112 microRNA 146a Homo sapiens 18-26 34052997-10 2021 In conclusion, these findings demonstrate that BMSC-derived exosomal miR-146a-5p regulates Th17/Treg imbalance in ITP by repressing IRAK1 expression. treg 96-100 microRNA 146a Homo sapiens 69-77 33340248-9 2021 MiR-146a was found inhibited the viability, proliferation and invasion of retinoblastoma cell by MTT, EdU, and transwell assays. monooxyethylene trimethylolpropane tristearate 97-100 microRNA 146a Homo sapiens 0-8 33445213-0 2021 The antioxidant and anti-inflammatory effects of astaxanthin supplementation on the expression of miR-146a and miR-126 in patients with type 2 diabetes mellitus: A randomized, double-blind, placebo-controlled clinical trial. astaxanthine 49-60 microRNA 146a Homo sapiens 98-106 33877886-0 2021 Long Noncoding RNA RP11-89K21.1 Interacts with miR-146a/b-5p to Promote Proliferation and Gefitinib Resistance Through Regulating RHPN2 and RhoA/ROCK Pathway in Lung Adenocarcinoma. Gefitinib 90-99 microRNA 146a Homo sapiens 47-57 33253979-8 2021 Furthermore, miR-21, miR-25, miR-27b, miR-19b, miR-125b, miR-146a and miR-210 predicted response to platinum based treatments. Platinum 100-108 microRNA 146a Homo sapiens 57-65 33753282-0 2021 Cerium oxide nanoparticle delivery of microRNA-146a for local treatment of acute lung injury. ceric oxide 0-12 microRNA 146a Homo sapiens 38-51 33724614-6 2021 In contrast, Oxygen-Ozone therapy notably decreased the expression level of miR-146a in treated patients. Oxygen 13-19 microRNA 146a Homo sapiens 76-84 33724614-6 2021 In contrast, Oxygen-Ozone therapy notably decreased the expression level of miR-146a in treated patients. Ozone 20-25 microRNA 146a Homo sapiens 76-84 33715884-12 2021 Moreover, the p38 MAPK signaling pathway and ROS production were activated upon stimulation with a miR-146a-5p mimic. Reactive Oxygen Species 45-48 microRNA 146a Homo sapiens 99-107 33715884-15 2021 This suggests that miR-146a increases Abeta deposition and ROS accumulation via the p-p38 signaling pathway. Reactive Oxygen Species 59-62 microRNA 146a Homo sapiens 19-27 33753282-3 2021 Nanoparticle technology with cerium oxide nanoparticles (CNP) offers a mechanism by which unstable therapeutics such as the anti-inflammatory microRNA-146a can be locally delivered to the injured lung without systemic uptake. ceric oxide 29-41 microRNA 146a Homo sapiens 142-155 33753282-4 2021 In this study, we evaluated the potential of the radical scavenging CNP conjugated to microRNA-146a (termed CNP-miR146a) in preventing acute lung injury (ALI) following exposure to bleomycin. Bleomycin 181-190 microRNA 146a Homo sapiens 86-99 33753282-4 2021 In this study, we evaluated the potential of the radical scavenging CNP conjugated to microRNA-146a (termed CNP-miR146a) in preventing acute lung injury (ALI) following exposure to bleomycin. Bleomycin 181-190 microRNA 146a Homo sapiens 112-119 33453674-2 2021 Hence, the study aimed to inspect the ability of the combination therapy of metformin and omega-3 to modulate different signaling pathways and micro RNAs such as (miR-155, miR-146a and miR-34) as new targets in order to mitigate adjuvant-induced arthritis and compare their effect to that of methotrexate. Metformin 76-85 microRNA 146a Homo sapiens 172-180 33620550-2 2021 This trial was, therefore, designed to determine CoQ10 efficacy on inflammation and antioxidant status, antimicrobial peptides, and microRNA-146a expression in UC patients. coenzyme Q10 49-54 microRNA 146a Homo sapiens 132-145 33565328-3 2021 Results: Lnc-MALAT1 negatively correlated with miR-125b, miR-146a and miR-203 Furthermore, lnc-MALAT1, miR-125b, miR-146a and miR-203 correlated with diabetes mellitus, hyperuricemia, lesion properties, cholesterol, inflammation and cardiac function indexes. Cholesterol 203-214 microRNA 146a Homo sapiens 113-121 33532131-0 2021 Hydrogen Peroxide-Induced Senescence Reduces the Wound Healing-Promoting Effects of Mesenchymal Stem Cell-Derived Exosomes Partially via miR-146a. Hydrogen Peroxide 0-17 microRNA 146a Homo sapiens 137-145 33532131-9 2021 Our study is the first to demonstrate that cell senescence induced by H2O2 alters the pro-angiogenic ability of exosomes by modulating the expression of exosomal miRNAs, especially miR-146a, thus providing new insights into the correlation between parental cell state and exosome content and function. Hydrogen Peroxide 70-74 microRNA 146a Homo sapiens 181-189 33172871-11 2021 This study reported for the first time that measurement of the circulating miR-146a expression at 14 days can predict the early response to imatinib treatment in patients with CML. Imatinib Mesylate 140-148 microRNA 146a Homo sapiens 75-83 32973101-4 2021 Further, miR-146a overexpression significantly inhibited the proliferation and invasion of GBM patient-derived primary cells and increased their response to temozolomide (TMZ), both in vitro and in vivo. Temozolomide 157-169 microRNA 146a Homo sapiens 9-17 33172871-0 2021 Circulating miR-146a expression predicts early treatment response to imatinib in adult chronic myeloid leukemia. Imatinib Mesylate 69-77 microRNA 146a Homo sapiens 12-20 33172871-1 2021 This study aimed to investigate the prognostic role of circulating miR-146a in the prediction of early response to imatinib treatment in patients with chronic myeloid leukemia (CML). Imatinib Mesylate 115-123 microRNA 146a Homo sapiens 67-75 33172871-4 2021 Circulating miR-146a levels were assessed by quantitative rt-PCR at days 0, 14 and 90 of imatinib therapy for patients and once for controls. Imatinib Mesylate 89-97 microRNA 146a Homo sapiens 12-20 33172871-8 2021 The circulating miR-146a level was significantly lower in patients with CML than in healthy subjects and showed a significant rise after 14 days of imatinib treatment and an inverse correlation with BCR-ABL expression levels at 90 days. Imatinib Mesylate 148-156 microRNA 146a Homo sapiens 16-24 33454992-0 2021 Resveratrol prevents steroid-induced osteonecrosis of the femoral head via miR-146a modulation. Resveratrol 0-11 microRNA 146a Homo sapiens 75-83 33454992-0 2021 Resveratrol prevents steroid-induced osteonecrosis of the femoral head via miR-146a modulation. Steroids 21-28 microRNA 146a Homo sapiens 75-83 33454992-7 2021 The results of our study suggest that Res prevents steroid-induced osteonecrosis by upregulating miR-146a, and thereby stabilizes osteogenesis/osteoclastogenesis homeostasis via Wnt/FOXO and Sirt1/NF-kappaB pathways. Steroids 51-58 microRNA 146a Homo sapiens 97-105 33129987-0 2021 Bone marrow stromal cells stimulated by strontium-substituted calcium silicate ceramics: release of exosomal miR-146a regulates osteogenesis and angiogenesis. calcium silicate 62-78 microRNA 146a Homo sapiens 109-117 33129987-6 2021 The results showed that Sr-CS-Exo could significantly promote in vitro angiogenesis of human umbilical vein endothelial cells (HUVECs), which might be attributed to elevated pro-angiogenic miR-146a cargos and inhibition of Smad4 and NF2 proteins. sr-cs 24-29 microRNA 146a Homo sapiens 189-197 32931869-0 2021 miR146a up-regulation is involved in small HA oligosaccharides-induced pro-inflammatory response in human chondrocytes. Oligosaccharides 46-62 microRNA 146a Homo sapiens 0-7 33002743-0 2021 miRNA-146a-5p mitigates stress-induced premature senescence of D-galactose-induced primary thymic stromal cells. Galactose 63-74 microRNA 146a Homo sapiens 0-10 32973101-4 2021 Further, miR-146a overexpression significantly inhibited the proliferation and invasion of GBM patient-derived primary cells and increased their response to temozolomide (TMZ), both in vitro and in vivo. Temozolomide 171-174 microRNA 146a Homo sapiens 9-17 32973101-5 2021 Mechanistically, miR-146a directly silenced POU3F2 and SMARCA5, two transcription factors that mutually regulated each other, significantly compromising GBM-stemness and increasing TMZ response. Temozolomide 181-184 microRNA 146a Homo sapiens 17-25 32973101-6 2021 Collectively, our data show that miR-146a-POU3F2/SMARCA5 pathway plays a critical role in suppressing GBM-stemness and increasing TMZ-response, suggesting that POU3F2 and SMARCA5 may serve as novel therapeutic targets in GBM. Temozolomide 130-133 microRNA 146a Homo sapiens 33-41 32981813-7 2020 Patients in the high baPWV group had higher plasma miR-146a levels than those in the normal baPWV group (3.43 +- 1.32 vs 1.98 +- 1.48, P < 0.001). bapwv 21-26 microRNA 146a Homo sapiens 51-59 33317606-10 2020 MiR-146a-5p level in exosomes from ETOH-treated CAFs was significantly reduced. Ethanol 35-39 microRNA 146a Homo sapiens 0-8 33317606-12 2020 CONCLUSIONS: CAFs-derived exosomal miR-146a-5p confers metastasis in PCa cells under ADT through the EGFR/ERK pathway and it may present a new treatment for PCa. adt 85-88 microRNA 146a Homo sapiens 35-43 33259730-0 2020 miR-146a Enhances the Sensitivity of Breast Cancer Cells to Paclitaxel by Downregulating IRAK1. Paclitaxel 60-70 microRNA 146a Homo sapiens 0-8 33259730-1 2020 Objective: To investigate the effect of miR-146a on the sensitivity of breast cancer cells to paclitaxel (PTX). Paclitaxel 94-104 microRNA 146a Homo sapiens 40-48 33259730-1 2020 Objective: To investigate the effect of miR-146a on the sensitivity of breast cancer cells to paclitaxel (PTX). Paclitaxel 106-109 microRNA 146a Homo sapiens 40-48 33259730-13 2020 Compared with MCF-7/PTX cells, the expression of miR-146a gene in MCF-7 cells was significantly increased, while the expression of IRAK1 gene was significantly reduced (p < 0.05). Paclitaxel 20-23 microRNA 146a Homo sapiens 49-57 33259730-17 2020 Conclusion: miR-146a can enhance the sensitivity of breast cancer cells to PTX; the mechanism may be related to the downregulation of IRAK1. Paclitaxel 75-78 microRNA 146a Homo sapiens 12-20 32777157-0 2020 Metformin andbetter survival in Type 2 Diabetes patients with NSCLC during EGFR-TKI Treatment: implications of miR-146a? Metformin 0-9 microRNA 146a Homo sapiens 111-119 32981813-9 2020 On binary logistic regression, plasma miR-146a level was an independent risk factor for thickened CIMT (OR = 3.890, 95% CI 1.415-7.698, P = 0.008) and high baPWV (OR = 1.954, 95% CI 1.256-3.040, P = 0.002) after adjustment for established cardiovascular risk factors. bapwv 156-161 microRNA 146a Homo sapiens 38-46 32981813-10 2020 The area under the receiver operating characteristics curve (AUROC) of plasma miR-146a level for predicting thickened CIMT was 0.795 (95%CI 0.708-0.883, P < 0.001) and for predicting high baPWV was 0.773 (95%CI 0.679-0.867, P < 0.001). bapwv 188-193 microRNA 146a Homo sapiens 78-86 31932355-7 2020 RESULTS: rs2910164 C/G in the seed region of miR-146a was associated with warfarin dose requirement (p<0.001); the patients with GG genotype had the higher mean dose of warfarin (40.6 mg/week, compared with 33.9 and 31.8 mg/week for GC and CC genotypes, respectively). Warfarin 74-82 microRNA 146a Homo sapiens 45-53 31932355-7 2020 RESULTS: rs2910164 C/G in the seed region of miR-146a was associated with warfarin dose requirement (p<0.001); the patients with GG genotype had the higher mean dose of warfarin (40.6 mg/week, compared with 33.9 and 31.8 mg/week for GC and CC genotypes, respectively). Warfarin 172-180 microRNA 146a Homo sapiens 45-53 31932355-9 2020 CONCLUSION: rs2910164 C/G in the seed region of miR-146a is associated with warfarin maintenance dose, likely by disrupting interaction between miR-146a and ATP-binding cassette subfamily B member 1 gene, ABCB1. Warfarin 76-84 microRNA 146a Homo sapiens 48-56 31932355-9 2020 CONCLUSION: rs2910164 C/G in the seed region of miR-146a is associated with warfarin maintenance dose, likely by disrupting interaction between miR-146a and ATP-binding cassette subfamily B member 1 gene, ABCB1. Warfarin 76-84 microRNA 146a Homo sapiens 144-152 32952629-0 2020 MicroRNA-146a downregulates the production of hyaluronic acid and collagen I in Graves" ophthalmopathy orbital fibroblasts. Hyaluronic Acid 46-61 microRNA 146a Homo sapiens 0-13 32952629-1 2020 The present study aimed to investigate the effect of microRNA (miR)-146a on the secretion of hyaluronic acid (HA) and collagen I in Graves" ophthalmopathy (GO) orbital fibroblasts, and identify potential novel targets for the clinical treatment of GO. Hyaluronic Acid 93-108 microRNA 146a Homo sapiens 53-72 33193424-2 2020 We have previously of radical scavenging cerium oxide nanoparticles (CNP) conjugated to the anti-inflammatory microRNA (miR)-146a, termed CNP-miR146a, improves diabetic wound healing by synergistically lowering oxidative stress and inflammation, and we sought to evaluate this treatment in a topical application. ceric oxide 41-53 microRNA 146a Homo sapiens 110-129 33095833-10 2020 Both miR-146a and miR-16-5p showed statistically significant association with 30-day mortality after admission due to CAP (1.10 vs. 0.23 and 51.74 vs. 35.23, respectively), and this association remained for miR-16-5p in the multivariate analysis adjusted for age, gender and history of bronchoaspiration (OR 0.95, p = 0.021). mir-16-5p 207-216 microRNA 146a Homo sapiens 5-13 33193424-2 2020 We have previously of radical scavenging cerium oxide nanoparticles (CNP) conjugated to the anti-inflammatory microRNA (miR)-146a, termed CNP-miR146a, improves diabetic wound healing by synergistically lowering oxidative stress and inflammation, and we sought to evaluate this treatment in a topical application. ceric oxide 41-53 microRNA 146a Homo sapiens 142-149 32356454-10 2020 Three miRNAs suppressed by colchicine (miR-146a, miR-17, miR-130a) were identified as regulators of inflammatory pathways. Colchicine 27-37 microRNA 146a Homo sapiens 39-47 32998457-9 2020 MiR-146a in Tregs is higher in rheumatoid factor (RF) positive RA patients. tregs 12-17 microRNA 146a Homo sapiens 0-8 32937997-3 2020 We demonstrated that while alcohol intoxication lowers anti-inflammatory miRNA (mir-146a-5p, mir-21-5p, mir-182-5p) levels in plasma EVs from human and mice female adolescents, these EV miRNAs increased in males. Alcohols 27-34 microRNA 146a Homo sapiens 80-88 32896208-4 2020 Overexpression of miR146a occurred in allopurinol-tolerant HLA-B*58:01 carriers. Allopurinol 38-49 microRNA 146a Homo sapiens 18-25 32648688-0 2020 CEACAM6 promotes cisplatin resistance in lung adenocarcinoma and is regulated by microRNA-146a and microRNA-26a. Cisplatin 17-26 microRNA 146a Homo sapiens 81-94 32626953-0 2020 Exosomal microRNA-146a derived from mesenchymal stem cells increases the sensitivity of ovarian cancer cells to docetaxel and taxane via a LAMC2-mediated PI3K/Akt axis. Docetaxel 112-121 microRNA 146a Homo sapiens 9-22 32626953-0 2020 Exosomal microRNA-146a derived from mesenchymal stem cells increases the sensitivity of ovarian cancer cells to docetaxel and taxane via a LAMC2-mediated PI3K/Akt axis. taxane 126-132 microRNA 146a Homo sapiens 9-22 32896208-6 2020 Overexpression of miR146a is potentially important for allopurinol tolerance in HLA-B*58:01 carriers. Allopurinol 55-66 microRNA 146a Homo sapiens 18-25 32944178-9 2020 miR-146a targets IRAK1, a serine-threonine kinase involved in IL-8 signalling. Serine 26-32 microRNA 146a Homo sapiens 0-8 32315958-2 2020 This study was conducted to investigate the effects of daily consumption of sodium butyrate (NaBut) and high-performance (HP) inulin supplementation, individually or in combination, on the expression of pyroptosis-related genes, microRNA (miR) 146a-5p, miR-9-5p and biomarkers of oxidative stress in patients with type 2 diabetes (T2DM). Butyric Acid 76-91 microRNA 146a Homo sapiens 229-248 32315958-2 2020 This study was conducted to investigate the effects of daily consumption of sodium butyrate (NaBut) and high-performance (HP) inulin supplementation, individually or in combination, on the expression of pyroptosis-related genes, microRNA (miR) 146a-5p, miR-9-5p and biomarkers of oxidative stress in patients with type 2 diabetes (T2DM). nabut 93-98 microRNA 146a Homo sapiens 229-248 32315958-9 2020 Furthermore, butyrate and concomitant use of butyrate and inulin caused a significant increase in the fold change of miR-146a and miR-9 compared with the placebo group (p < 0.05). Butyrates 13-21 microRNA 146a Homo sapiens 117-125 32315958-9 2020 Furthermore, butyrate and concomitant use of butyrate and inulin caused a significant increase in the fold change of miR-146a and miR-9 compared with the placebo group (p < 0.05). Butyrates 45-53 microRNA 146a Homo sapiens 117-125 32315958-11 2020 CONCLUSION: In summary, the change in expression level of miR-146a-5p and miR-9-5p due to butyrate supplementation may have a pivotal role in alleviating of diabetes via inhibiting pyroptosis by targeting TLR2 and NF-kappaB1. Butyrates 90-98 microRNA 146a Homo sapiens 58-66 31872268-9 2020 CONCLUSION: In conclusion, a recent exposure to certain metals, mainly chromium and nickel, appears to be associated to a decrease in plasma expression of miR-21, miR-146a and miR-155. Chromium 71-79 microRNA 146a Homo sapiens 163-171 31872268-9 2020 CONCLUSION: In conclusion, a recent exposure to certain metals, mainly chromium and nickel, appears to be associated to a decrease in plasma expression of miR-21, miR-146a and miR-155. Nickel 84-90 microRNA 146a Homo sapiens 163-171 32572893-13 2020 The frequency of CC+CA in the dominant model of IRAK1 rs3027898 and that of TG+GG in the recessive model of miR-146a rs7702165 in disease group were lower than those in control group. Thioguanine 76-78 microRNA 146a Homo sapiens 108-116 32216502-0 2020 Quercetin suppresses migration and invasion by targeting miR-146a/GATA6 axis in fibroblast-like synoviocytes of rheumatoid arthritis. Quercetin 0-9 microRNA 146a Homo sapiens 57-65 32216502-8 2020 The correlation between miR-146a and GATA6 was validated using luciferase reporter assay.Results: Transwell assay revealed that the migration and invasion of FLSs were significantly inhibited after quercetin treatment, which was also proved by decreased expression of F-actin. Quercetin 198-207 microRNA 146a Homo sapiens 24-32 32216502-10 2020 Quercetin treatment elevated the RNA level of miR-146a, but suppressed the expression of GATA6 in FLSs. Quercetin 0-9 microRNA 146a Homo sapiens 46-54 32216502-13 2020 In addition, specific anti-miR-146a inhibitor abolished quercetin-mediated suppression of migration and invasion of FLSs.Conclusion: Our study suggested that quercetin suppresses the migration and invasion of FLSs via regulating the miR-146a/GATA6 axis. Quercetin 56-65 microRNA 146a Homo sapiens 27-35 32216502-13 2020 In addition, specific anti-miR-146a inhibitor abolished quercetin-mediated suppression of migration and invasion of FLSs.Conclusion: Our study suggested that quercetin suppresses the migration and invasion of FLSs via regulating the miR-146a/GATA6 axis. Quercetin 56-65 microRNA 146a Homo sapiens 233-241 32216502-13 2020 In addition, specific anti-miR-146a inhibitor abolished quercetin-mediated suppression of migration and invasion of FLSs.Conclusion: Our study suggested that quercetin suppresses the migration and invasion of FLSs via regulating the miR-146a/GATA6 axis. Quercetin 158-167 microRNA 146a Homo sapiens 27-35 32216502-13 2020 In addition, specific anti-miR-146a inhibitor abolished quercetin-mediated suppression of migration and invasion of FLSs.Conclusion: Our study suggested that quercetin suppresses the migration and invasion of FLSs via regulating the miR-146a/GATA6 axis. Quercetin 158-167 microRNA 146a Homo sapiens 233-241 32223462-0 2020 The role of beta-d-mannuronic acid, as a new non-steroidal anti-inflammatory drug on expression of miR-146a, IRAK1, TRAF6, NF-kappaB and pro-inflammatory cytokines following a clinical trial in rheumatoid arthritis patients. mannuronic acid 12-34 microRNA 146a Homo sapiens 99-107 32481361-8 2020 Besides, MiR-146a and miR-146b expressions were positively correlated with acute pathologic and chronic health evaluation II score, sequential organ failure assessment score, serum creatinine, C-reactive protein, tumor necrosis factor-alpha, interleukin (IL)-1beta, IL-6, IL-17, while negatively correlated with albumin. Creatinine 181-191 microRNA 146a Homo sapiens 9-17 31843406-8 2020 Additionally, let-7a, miR-146a-5p, and miR-155-5p were found to mediate the associations of BPDE-Alb adducts with IL-6 and/or TLR2 expression. 7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide 92-96 microRNA 146a Homo sapiens 22-30 32125286-8 2020 To validate our preclinical findings in patients, we analyzed the impact of a SNP in the MIR146A gene on irAE severity in 167 patients treated with ICIs. icis 148-152 microRNA 146a Homo sapiens 89-96 32207596-11 2022 Low dose curcumin can significantly reduce the level of neuropro-inflammatory miR-146A, up-regulate the expression of CFH protein, inhibit the phenotype of M1 microglia, and play a role in the treatment of AD by promoting the phagocytosis and clearance mechanism of A beta. Curcumin 9-17 microRNA 146a Homo sapiens 78-86 32210951-11 2020 Indeed, an effect of prednisone on miR-146a expression was demonstrated in vitro on peripheral blood cells. Prednisone 21-31 microRNA 146a Homo sapiens 35-43 31982837-16 2020 Quercetin having anti-cancer activity induce the apoptosis through regulating miR-16, 26b, 34a, let-7g, 125a and miR-605 and reduce the miRNA expression like miR-146a/b, 503 and 194 which are involved in metastasis. Quercetin 0-9 microRNA 146a Homo sapiens 158-168 31986004-3 2020 Here, we report a pH/ATP-activated nanocomplexes for increasing cytosolic delivery of miR146a which can effectively inhibit the expression of epidermal growth factor receptor (EGFR) in AIPC. Adenosine Triphosphate 21-24 microRNA 146a Homo sapiens 86-93 32117283-6 2020 We studied the effects of Meth on IL-1beta and miR-146a, a well-characterized member of the innate immune signaling network. Methamphetamine 26-30 microRNA 146a Homo sapiens 47-55 32117283-7 2020 We found that Meth induces miR-146a and triggers an IL-1beta auto-regulatory loop to modulate innate immune signaling in CD4+ T-cells. Methamphetamine 14-18 microRNA 146a Homo sapiens 27-35 32125286-10 2020 Furthermore, we identified the MIR146A SNP rs2910164 as a biomarker to predict severe irAE development in ICI-treated patients. ici 106-109 microRNA 146a Homo sapiens 31-38 31715376-0 2020 Label-free sensing platform for miRNA-146a based on chromo-fluorogenic pyrophosphate recognition. diphosphoric acid 71-84 microRNA 146a Homo sapiens 32-42 31715376-1 2020 In this study we applied the dual-responsive chromo-fluorescent Cu2+ chelate 1C for the recognition of miRNA-146a through a pyrophosphate (PPi) sensing strategy in a rolling circle amplification (RCA) process. cupric ion 64-68 microRNA 146a Homo sapiens 103-113 31715376-1 2020 In this study we applied the dual-responsive chromo-fluorescent Cu2+ chelate 1C for the recognition of miRNA-146a through a pyrophosphate (PPi) sensing strategy in a rolling circle amplification (RCA) process. diphosphoric acid 124-137 microRNA 146a Homo sapiens 103-113 31715376-5 2020 We also report a label-free approach for monitoring miRNA-146a amplification in an RCA process under modified T4 ligase and phi29 buffer conditions, using the Cu2+ ensemble 1C at pH 7.0 (4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid: HEPES, 10 mM MgCl2); the time required to perform this process (40-50 min) was relatively shorter than conventional RCA process. phi29 124-129 microRNA 146a Homo sapiens 52-62 31715376-5 2020 We also report a label-free approach for monitoring miRNA-146a amplification in an RCA process under modified T4 ligase and phi29 buffer conditions, using the Cu2+ ensemble 1C at pH 7.0 (4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid: HEPES, 10 mM MgCl2); the time required to perform this process (40-50 min) was relatively shorter than conventional RCA process. cupric ion 159-163 microRNA 146a Homo sapiens 52-62 31715376-5 2020 We also report a label-free approach for monitoring miRNA-146a amplification in an RCA process under modified T4 ligase and phi29 buffer conditions, using the Cu2+ ensemble 1C at pH 7.0 (4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid: HEPES, 10 mM MgCl2); the time required to perform this process (40-50 min) was relatively shorter than conventional RCA process. TVZ 7 187-237 microRNA 146a Homo sapiens 52-62 31715376-5 2020 We also report a label-free approach for monitoring miRNA-146a amplification in an RCA process under modified T4 ligase and phi29 buffer conditions, using the Cu2+ ensemble 1C at pH 7.0 (4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid: HEPES, 10 mM MgCl2); the time required to perform this process (40-50 min) was relatively shorter than conventional RCA process. HEPES 239-244 microRNA 146a Homo sapiens 52-62 31715376-5 2020 We also report a label-free approach for monitoring miRNA-146a amplification in an RCA process under modified T4 ligase and phi29 buffer conditions, using the Cu2+ ensemble 1C at pH 7.0 (4-(2-hydroxyethyl)piperazine-1-ethanesulfonic acid: HEPES, 10 mM MgCl2); the time required to perform this process (40-50 min) was relatively shorter than conventional RCA process. Magnesium Chloride 252-257 microRNA 146a Homo sapiens 52-62 31805184-3 2020 Here, we describe a myeloid cell-selective NF-kappaB inhibitor using an miR-146a mimic oligonucleotide conjugated to a scavenger receptor/Toll-like receptor 9 agonist (C-miR146a). Oligonucleotides 87-102 microRNA 146a Homo sapiens 72-80 31111958-3 2019 Here, we show that the histone deacetylase inhibitor, trichostatin A (TSA), suppresses HER2-overexpressing breast cancer via upregulation of miR-146a and the resultant repression of its oncogenic targets, interleukin-1 receptor-associated kinase 1 and the chemokine receptor CXCR4. trichostatin A 54-68 microRNA 146a Homo sapiens 141-149 31074089-9 2020 The RT-PCR data indicated that the expression of miR-17 and miR-27 were significantly decreased following nanocurcumin treatment while miR-146a and FoxP3 were significantly increased. nanocurcumin 106-118 microRNA 146a Homo sapiens 135-143 31111958-3 2019 Here, we show that the histone deacetylase inhibitor, trichostatin A (TSA), suppresses HER2-overexpressing breast cancer via upregulation of miR-146a and the resultant repression of its oncogenic targets, interleukin-1 receptor-associated kinase 1 and the chemokine receptor CXCR4. trichostatin A 70-73 microRNA 146a Homo sapiens 141-149 31425002-7 2019 miR-146a-5p mimic transfection downregulated arachidonic acid metabolism genes, the RNA-binding protein HuR, and many HuR-stabilized pro-cancer mRNAs, including TGF-beta, HIF-1alpha, and various cyclins. Arachidonic Acid 45-61 microRNA 146a Homo sapiens 0-8 31866771-8 2019 The miR-146a expression in PBMCs was higher in SAP, UAP, and AMI groups than in CPS group. 4-Deoxy-2-O-Sulfo-Alpha-L-Threo-Hex-4-Enopyranuronic Acid 52-55 microRNA 146a Homo sapiens 4-12 31588496-5 2019 In particular, the miR-548e-5p inhibitor induced apoptosis, while tumor necrosis factor receptor-associated factor 6, a predicted target of miR-146a-5p and miR-548e-5p, was involved in the regulation of oxidative stress in the human trophoblast cells. mir-548e-5p 19-30 microRNA 146a Homo sapiens 140-148 31727077-8 2019 Consistent increase of miR-21 and miR-146a/b was found in Gd+ MS patients. Gadolinium 58-60 microRNA 146a Homo sapiens 34-42 31538427-2 2019 This study aimed to investigate the effect of miR-146a on childhood AL and its underlying molecular mechanisms. Aluminum 68-70 microRNA 146a Homo sapiens 46-54 31595849-0 2019 Renoprotective effect of curcumin labelled on Mesoscale Nanoparticles (MNPs) on Renal Ischemia-Reperfusion Injury (RIRI) via the miR-146a/nNOS/NO/cGMP/PKG signaling pathway. Curcumin 25-33 microRNA 146a Homo sapiens 129-137 31595849-5 2019 Finally, the effect of Curcumin on the transcriptional efficiencies of miR-146a, nNOS, eNOS and iNOS was studied using luciferase assay. Curcumin 23-31 microRNA 146a Homo sapiens 71-79 31595849-10 2019 Moreover, Curcumin enhanced miR-146a expression, while reducing the expression of nNOS, iNOS, cGPM, caspase-3 and PKG as well as the synthesis of NO. Curcumin 10-18 microRNA 146a Homo sapiens 28-36 31595849-11 2019 Curcumin may exert its effect by reducing the transcriptional efficiency of iNOS promoter, while increasing the transcriptional efficiency of miR-146a promoter. Curcumin 0-8 microRNA 146a Homo sapiens 142-150 31595849-13 2019 The protective effect of Curcumin against RIRI may be mediated by its regulation of cell apoptosis through the miR-146a/nNOS/NO/cGMP/PKG signaling pathway. Curcumin 25-33 microRNA 146a Homo sapiens 111-119 31595849-13 2019 The protective effect of Curcumin against RIRI may be mediated by its regulation of cell apoptosis through the miR-146a/nNOS/NO/cGMP/PKG signaling pathway. 3'-guanylic acid 128-132 microRNA 146a Homo sapiens 111-119 31319144-2 2019 In this study, Nanocomposite Microparticles (NCMPs) of microRNA (miR-146a) containing PGA-co-PDL nanoparticles (NPs) for dry powder inhalation were formulated using l-leucine and mannitol. Prostaglandins A 86-89 microRNA 146a Homo sapiens 55-73 31319144-8 2019 These results indicate the optimal process parameters for the preparation of NCMPs of miR-146a-containing PGA-co-PDL NPs suitable for inhalation in the treatment and management of COPD. Prostaglandins A 106-109 microRNA 146a Homo sapiens 86-94 31416388-10 2019 Importantly, exosomal miR-146a secreted by oxLDL-treated macrophages promoted ROS and NETs release via targeting SOD2. Reactive Oxygen Species 78-81 microRNA 146a Homo sapiens 22-30 31584250-8 2019 Furthermore, inflammation-related microRNAs miR-16, miR-146a, miR-125b, and miR-155 are altered in response to AOH. alternariol 111-114 microRNA 146a Homo sapiens 52-60 31072418-0 2019 Triptolide inhibits breast cancer cell metastasis through inducing the expression of miR-146a, a negative regulator of Rho GTPase. triptolide 0-10 microRNA 146a Homo sapiens 85-93 31072418-5 2019 miRNAome variation in MDA-MB-231 cells with or without triptolide treatment demonstrated that miR-146a was upregulated following treatment with triptolide. triptolide 55-65 microRNA 146a Homo sapiens 94-102 31072418-5 2019 miRNAome variation in MDA-MB-231 cells with or without triptolide treatment demonstrated that miR-146a was upregulated following treatment with triptolide. triptolide 144-154 microRNA 146a Homo sapiens 94-102 31072418-11 2019 Triptolide combined with miR-146a could improve the effect of triptolide treatment on breast cancer. triptolide 62-72 microRNA 146a Homo sapiens 25-33 30546074-9 2019 Moreover, the expression of microRNAs (miR)-144/451, miR-146a, miR-155, and miR-223 was also modulated by TNFalpha and ceramide treatments, in line with cellular observations. Ceramides 119-127 microRNA 146a Homo sapiens 53-61 31295570-3 2019 Available experimental studies indicate that quercetin could modulate multiple cancer-relevant miRNAs including let-7, miR-21, miR-146a and miR-155, thereby inhibiting cancer initiation and development. Quercetin 45-54 microRNA 146a Homo sapiens 127-135 31507414-9 2019 Cardiac-specific overexpression of miR-146a prevented the deteriorate effect of SNT on calcium transients, thereby alleviating the decreased contractility of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs). Calcium 87-94 microRNA 146a Homo sapiens 35-43 31434993-0 2019 Isosteviol Sodium Protects against Ischemic Stroke by Modulating Microglia/Macrophage Polarization via Disruption of GAS5/miR-146a-5p sponge. isosteviol sodium 0-17 microRNA 146a Homo sapiens 122-130 31434993-7 2019 Taken together, the present study demonstrated that STV-Na exerted neuroprotective effects by modulating microglia/macrophage polarization in ischemic stroke via the GAS5/miR-146a-5p sponge. Stavudine 52-55 microRNA 146a Homo sapiens 171-179 31077718-5 2019 The methylation status of miR-140 and miR-146a regulatory regions was analyzed using qMSP and bisulfite sequencing analysis. hydrogen sulfite 94-103 microRNA 146a Homo sapiens 38-46 31431821-7 2019 Quercetin has been effective in modulating miR-146a. Quercetin 0-9 microRNA 146a Homo sapiens 43-51 31077718-12 2019 Similarly, 5-AzadC-treated OA synoviocytes showed decreased expression of IRAK-1, IL1Beta and IL-6, which was reversed following 5-AzadC-/miR-146a inhibitor treatment. Decitabine 11-18 microRNA 146a Homo sapiens 138-146 31077718-12 2019 Similarly, 5-AzadC-treated OA synoviocytes showed decreased expression of IRAK-1, IL1Beta and IL-6, which was reversed following 5-AzadC-/miR-146a inhibitor treatment. Decitabine 129-136 microRNA 146a Homo sapiens 138-146 31077718-9 2019 5-AzadC-induced miR-140-5p and miR-146a upregulation was observed in OA chondrocytes and synoviocytes. Decitabine 0-7 microRNA 146a Homo sapiens 31-39 31316517-15 2019 RA miR-146a was associated with greater concentrations of cardiometabolic risk markers (plasma short-chain dicarboxyl/hydroxyl acylcarnitines, triglycerides, large VLDL particles, and small HDL particles) and lower concentrations of muscle energy substrates (long-chain acylcarnitines and pyruvate). dicarboxyl 107-117 microRNA 146a Homo sapiens 3-11 30880174-3 2019 When a gender-stratified analysis was ran, the miR-146a age-related trajectory was confirmed only in men and a negative correlation with PAI-1, uric acid, and creatinine was also observed. Uric Acid 144-153 microRNA 146a Homo sapiens 47-55 31316517-15 2019 RA miR-146a was associated with greater concentrations of cardiometabolic risk markers (plasma short-chain dicarboxyl/hydroxyl acylcarnitines, triglycerides, large VLDL particles, and small HDL particles) and lower concentrations of muscle energy substrates (long-chain acylcarnitines and pyruvate). acylcarnitine 127-141 microRNA 146a Homo sapiens 3-11 31316517-15 2019 RA miR-146a was associated with greater concentrations of cardiometabolic risk markers (plasma short-chain dicarboxyl/hydroxyl acylcarnitines, triglycerides, large VLDL particles, and small HDL particles) and lower concentrations of muscle energy substrates (long-chain acylcarnitines and pyruvate). Triglycerides 143-156 microRNA 146a Homo sapiens 3-11 31316517-15 2019 RA miR-146a was associated with greater concentrations of cardiometabolic risk markers (plasma short-chain dicarboxyl/hydroxyl acylcarnitines, triglycerides, large VLDL particles, and small HDL particles) and lower concentrations of muscle energy substrates (long-chain acylcarnitines and pyruvate). acylcarnitine 270-284 microRNA 146a Homo sapiens 3-11 31316517-15 2019 RA miR-146a was associated with greater concentrations of cardiometabolic risk markers (plasma short-chain dicarboxyl/hydroxyl acylcarnitines, triglycerides, large VLDL particles, and small HDL particles) and lower concentrations of muscle energy substrates (long-chain acylcarnitines and pyruvate). Pyruvic Acid 289-297 microRNA 146a Homo sapiens 3-11 30880174-3 2019 When a gender-stratified analysis was ran, the miR-146a age-related trajectory was confirmed only in men and a negative correlation with PAI-1, uric acid, and creatinine was also observed. Creatinine 159-169 microRNA 146a Homo sapiens 47-55 30880174-4 2019 In women, miR-146a circulating levels showed negative correlations with azotemia, uric acid, waist/hip ratio and ferritin. Uric Acid 82-91 microRNA 146a Homo sapiens 10-18 30880174-6 2019 Significant positive correlations were found between miR-146a in diabetic patients and total cholesterol, LDL-C, ApoA1, ApoB, and platelets, and negative correlations with serum iron and ferritin. Cholesterol 93-104 microRNA 146a Homo sapiens 53-61 30880174-7 2019 Notably, miR-146a was significantly overexpressed in T2DM patients treated with metformin. Metformin 80-89 microRNA 146a Homo sapiens 9-17 30880174-8 2019 MiR-146a levels were significantly lower in diabetic patients than in age-matched CTR and negatively correlated to both fasting glucose and HbA1c in males. Glucose 128-135 microRNA 146a Homo sapiens 0-8 30710793-7 2019 Additionally, miR-146a-induced CXCL16 expression was blocked by TAK-242. ethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylate 64-71 microRNA 146a Homo sapiens 14-22 30833583-11 2019 The uptake of fluorescein and 64Cu labeled anti-miR-146a PNAs was higher than that of the negative control scramble PNAs in miRNA expressing cells in vitro. Copper-64 30-34 microRNA 146a Homo sapiens 48-56 30511295-11 2019 Receiver operating characteristic curve analysis showed that all three miRNAs were also good predictors of MTX response, showing the following values: hsa-miR-132-3p (area under curve (AUC) 0.756, P < 0.05), hsa-miR-146a-5p (AUC 0.760, P < 0.05), and hsa-miR-155-5p (AUC 0.728, P = 0.002). Methotrexate 107-110 microRNA 146a Homo sapiens 215-223 30511295-12 2019 CONCLUSION: hsa-miR-132-3p, hsa-miR-146a-5p, and hsa-miR-155-5p are potential biomarkers of responsiveness to MTX therapy. Methotrexate 110-113 microRNA 146a Homo sapiens 32-40 30615927-3 2019 In this study miR146a was adsorbed onto poly (glycerol adipate-co-omega-pentadecalactone), PGA-co-PDL, nanoparticles (NPs) to reduce target gene IRAK1 expression. poly 40-44 microRNA 146a Homo sapiens 14-21 30615927-3 2019 In this study miR146a was adsorbed onto poly (glycerol adipate-co-omega-pentadecalactone), PGA-co-PDL, nanoparticles (NPs) to reduce target gene IRAK1 expression. Prostaglandins A 91-94 microRNA 146a Homo sapiens 14-21 30615927-3 2019 In this study miR146a was adsorbed onto poly (glycerol adipate-co-omega-pentadecalactone), PGA-co-PDL, nanoparticles (NPs) to reduce target gene IRAK1 expression. -pdl 97-101 microRNA 146a Homo sapiens 14-21 30615927-10 2019 In conclusion, miR-146a was successfully adsorbed onto PGA-co-PDL-DOTAP NPs and the miR-146a retained biological activity. Prostaglandins A 55-58 microRNA 146a Homo sapiens 15-23 30615927-10 2019 In conclusion, miR-146a was successfully adsorbed onto PGA-co-PDL-DOTAP NPs and the miR-146a retained biological activity. Prostaglandins A 55-58 microRNA 146a Homo sapiens 84-92 30615927-11 2019 Therefore, these results demonstrate the potential of PGA-co-PDL NPs as a delivery system for miR-146a to treat COPD. Prostaglandins A 54-57 microRNA 146a Homo sapiens 94-102 30580082-7 2019 Hsa-miR-23a-3p, hsa-miR-16-5p, hsa-miR-146a-5p and hsa-miR-21-5p were identified in 2 or more trials as being able to differentiate patients who would remit with duloxetine treatment using samples collected before treatment initiation, suggesting that they may be good candidates for identification of predictive biomarkers of duloxetine response. Duloxetine Hydrochloride 162-172 microRNA 146a Homo sapiens 31-43 30859103-19 2019 Five miRs, miR-122, let7f, miR-21, miR-29a, and miR-146a, were reduced in the blood EVs from the EtOH w/o LI group, vs. no EtOH (p < 0.05). Ethanol 97-101 microRNA 146a Homo sapiens 48-56 30988678-5 2019 The aim of the present study was to compare the expression level of miR-146a in plasma-derived exosomes of responsive DLBCL patients (response to R-CHOP (Rituximab, and Cyclophosphamide, Hydroxydaunorubicin, Oncovine and Prednisone)), refractory DLBCL patients (resistant to R-CHOP), patients receiving R-CHOP, and healthy donors. Doxorubicin 187-206 microRNA 146a Homo sapiens 68-76 30988678-5 2019 The aim of the present study was to compare the expression level of miR-146a in plasma-derived exosomes of responsive DLBCL patients (response to R-CHOP (Rituximab, and Cyclophosphamide, Hydroxydaunorubicin, Oncovine and Prednisone)), refractory DLBCL patients (resistant to R-CHOP), patients receiving R-CHOP, and healthy donors. Prednisone 221-231 microRNA 146a Homo sapiens 68-76 30768595-3 2019 miR-146a is reduced in obese and type 2 diabetic patients and our results reveal that miR-146a-/- mice fed a high-fat diet (HFD) have exaggerated weight gain, increased adiposity, hepatosteatosis, and dysregulated blood glucose levels compared to wild-type controls. Glucose 220-227 microRNA 146a Homo sapiens 86-94 30720149-11 2019 The results of alizarin red staining showed that the deposition of calcium obviously increased in miR-146a-mimic group compared with that in miR-NC group, indicating that the osteogenic differentiation ability is significantly enhanced, while it markedly decreased in miR-146a-inhibitor group compared with that in miR-NC group. alizarin 15-27 microRNA 146a Homo sapiens 98-106 30720149-11 2019 The results of alizarin red staining showed that the deposition of calcium obviously increased in miR-146a-mimic group compared with that in miR-NC group, indicating that the osteogenic differentiation ability is significantly enhanced, while it markedly decreased in miR-146a-inhibitor group compared with that in miR-NC group. Calcium 67-74 microRNA 146a Homo sapiens 98-106 30720149-11 2019 The results of alizarin red staining showed that the deposition of calcium obviously increased in miR-146a-mimic group compared with that in miR-NC group, indicating that the osteogenic differentiation ability is significantly enhanced, while it markedly decreased in miR-146a-inhibitor group compared with that in miR-NC group. Calcium 67-74 microRNA 146a Homo sapiens 268-276 30145362-0 2018 miR-146a is involved in the regulation of vertebrate LC-PUFA biosynthesis by targeting elovl5 as demonstrated in rabbitfish Siganus canaliculatus. Fatty Acids, Unsaturated 56-60 microRNA 146a Homo sapiens 0-8 29484526-8 2018 Moreover, anti-miR-146a-mediated suppression on cell cytotoxicity was abated following MCL1 knockdown in H2O2-induced PC12 cells. Hydrogen Peroxide 105-109 microRNA 146a Homo sapiens 15-23 30145362-4 2018 The expression of miR-146a displayed an inverse pattern with that of elongase 5 (Elovl5), a key enzyme catalyzing the elongation of C18 (18:4n3 and 18:3n6) and C20 (20:5n3 and 20:4n6) PUFA in the LC-PUFA biosynthesis, in vivo in liver of rabbitfish reared under different salinities, as well as in vitro in S. canaliculatus hepatocyte line (SCHL) cells incubated with different fatty acids. Fatty Acids 378-389 microRNA 146a Homo sapiens 18-26 30175388-8 2018 Concomitantly, AOH (2-20 microM) affected the transcription levels of miR-146a and miR-155 in LPS-stimulated THP-1 derived macrophages dose-dependently by down- and upregulation, respectively. alternariol 15-18 microRNA 146a Homo sapiens 70-78 30212608-6 2018 Waist circumference, the inflammatory cytokine IL-8 and lipid parameters, principally total cholesterol, showed the strongest correlation with both the baseline levels and post-intervention correction of miR-146a-5p. Cholesterol 92-103 microRNA 146a Homo sapiens 204-212 30321140-7 2018 RESULTS The miR-146a C>G polymorphism was remarkably different (CC vs. CG+GG: P=0.027; CC+CG vs. GG: P=0.020; C vs. G: P=0.006). cysteinylglycine 74-76 microRNA 146a Homo sapiens 12-20 30321140-7 2018 RESULTS The miR-146a C>G polymorphism was remarkably different (CC vs. CG+GG: P=0.027; CC+CG vs. GG: P=0.020; C vs. G: P=0.006). cysteinylglycine 93-95 microRNA 146a Homo sapiens 12-20 29913408-11 2018 Further, inhibition of miR-146a abolished the protective effect of tripterine on cell damage triggered by LPS. celastrol 67-77 microRNA 146a Homo sapiens 23-31 30245930-4 2018 In the present study, the effect of the combined treatment of MBIC and doxorubicin on the expression level of several miRNAs including miR-34a, miR-146a, miR-320a and miR-542 were evaluated in MCF-7 and MDA-MB-231 breast cancer cell lines. Doxorubicin 71-82 microRNA 146a Homo sapiens 144-152 30254683-5 2018 Treatment of hUCB-MSCs with CoCl2 leads to increased expression of microRNA- (miR-) 146a, which was reported to modulate anti-inflammatory responses. cobaltous chloride 28-33 microRNA 146a Homo sapiens 67-88 30254683-6 2018 Hypoxia-inducible factor- (HIF-) 1alpha silencing and ERK inhibition abolished CoCl2-induced miR-146a expression, suggesting that ERK and HIF-1alpha signals are required for CoCl2-induced miR-146a expression in hUCB-MSCs. cobaltous chloride 79-84 microRNA 146a Homo sapiens 93-101 30254683-6 2018 Hypoxia-inducible factor- (HIF-) 1alpha silencing and ERK inhibition abolished CoCl2-induced miR-146a expression, suggesting that ERK and HIF-1alpha signals are required for CoCl2-induced miR-146a expression in hUCB-MSCs. cobaltous chloride 79-84 microRNA 146a Homo sapiens 188-196 30254683-6 2018 Hypoxia-inducible factor- (HIF-) 1alpha silencing and ERK inhibition abolished CoCl2-induced miR-146a expression, suggesting that ERK and HIF-1alpha signals are required for CoCl2-induced miR-146a expression in hUCB-MSCs. cobaltous chloride 174-179 microRNA 146a Homo sapiens 93-101 30254683-7 2018 These data suggest that treatment with CoCl2 enhances the immunosuppressive capacity of hUCB-MSCs through the ERK-HIF-1alpha-miR-146a-mediated signaling pathway. cobaltous chloride 39-44 microRNA 146a Homo sapiens 125-133 29913408-0 2018 Tripterine alleviates LPS-induced inflammatory injury by up-regulation of miR-146a in HaCaT cells. celastrol 0-10 microRNA 146a Homo sapiens 74-82 29913408-12 2018 Finally, tripterine deactivated JNK and NF-kappaB pathways through up-regulation of miR-146a. celastrol 9-19 microRNA 146a Homo sapiens 84-92 29913408-13 2018 CONCLUSION: These results demonstrated that tripterine could attenuate LPS-induced inflammatory injury and deactivate JNK and NF-kappaB pathways by up-regulation of miR-146a. celastrol 44-54 microRNA 146a Homo sapiens 165-173 29946002-5 2018 IL-1beta induced lower MIR146A expression in asthma-derived ASMCs compared with controls. asmcs 60-65 microRNA 146a Homo sapiens 23-30 29883261-7 2018 Both vamorolone and prednisolone returned these toward wild-type levels (miR-142-5p, miR-142-3p, miR-146a, miR-301a, miR-324-3p, miR-455-5p, miR-455-3p, miR-497, miR-652). Prednisolone 20-32 microRNA 146a Homo sapiens 97-105 29983589-8 2018 In the subgroup analyses, after adjustment by sex, age, alcohol consumption, and smoking status, results of multiple logistic regression analysis indicated that miRNA-146a rs2910164 C>G polymorphism increased the risk of EGJA in males, females, <64 years old, >=64 years old, never smoking, and never drinking subgroups. Alcohols 56-63 microRNA 146a Homo sapiens 161-171 30054544-7 2018 Up-regulation of miR-146a by CyP alone, affects subsequent cell response in term of TNF-alpha production even when monocytes are incubated with other TLR ligands, as lipoteichoic acid (LTA), thus confirming miR-146a as a critical player mediating TNF-alpha regulation during cross-tolerance with CyP. lipoteichoic acid 166-183 microRNA 146a Homo sapiens 17-25 30054544-7 2018 Up-regulation of miR-146a by CyP alone, affects subsequent cell response in term of TNF-alpha production even when monocytes are incubated with other TLR ligands, as lipoteichoic acid (LTA), thus confirming miR-146a as a critical player mediating TNF-alpha regulation during cross-tolerance with CyP. lipoteichoic acid 185-188 microRNA 146a Homo sapiens 17-25 29484780-3 2018 We found that compared with the C allele, the rs2910164 G allele of pre-miR-146a was associated with an increased risk of NSOC (additive model: odds ratio [OR] = 1.17, 95% confidence interval [CI]: 1.06-1.30, P = 0.002), including both cleft lip with or without cleft palate (CL/P) and cleft palate only (CPO). cpo 305-308 microRNA 146a Homo sapiens 72-80 29896267-8 2018 In addition, miR-146a expression in patients with paraquat poisoning-induced lung injury was significantly reduced in comparison with that in healthy subjects. Paraquat 50-58 microRNA 146a Homo sapiens 13-21 29896267-11 2018 Therefore, the present study demonstrated that increased expression of IL-6 in patients with lung injury caused by paraquat poisoning is associated with decreased expression of miR-146a. Paraquat 115-123 microRNA 146a Homo sapiens 177-185 29928483-0 2018 miR-146a suppresses 5-lipoxygenase activating protein (FLAP) expression and Leukotriene B4 production in lung cancer cells. Leukotrienes 76-87 microRNA 146a Homo sapiens 0-8 29928483-9 2018 Restoration of miR-146a also results in decreased cancer cell Leukotriene B4 (LTB4) production. Leukotriene B4 62-76 microRNA 146a Homo sapiens 15-23 29928483-11 2018 Taken together, this study and previous work from our lab suggest miR-146a is an endogenous dual inhibitor of AA metabolism in lung cancer cells by regulating both PG and LT production through direct targeting of the COX-2 and FLAP 3" UTRs. Prostaglandins 164-166 microRNA 146a Homo sapiens 66-74 29495389-2 2018 In this study, we analyzed the impact of miR-146a on the expression and function of NIS and on the overall survival of thyroid cancer patients. Nickel 84-87 microRNA 146a Homo sapiens 41-49 28528141-13 2018 Although the OIM or PC treatment upregulated miR-21, miR-29b, and miR-146a, only miR-146a was able to be induced by PC in combination with OIM. pc 20-22 microRNA 146a Homo sapiens 66-74 28528141-14 2018 CONCLUSION: This study demonstrated that PC enhances the differentiation of PDL cells, especially osteogenic through miR-146a upregulation. pc 41-43 microRNA 146a Homo sapiens 117-125 29328400-5 2018 In HK-2 cells, overexpression of miR-146a inhibited Nox4 protein expression and decreased reactive oxygen species (ROS) generation, oxidative stress and inflammation, and suppressed vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) protein expression. Reactive Oxygen Species 90-113 microRNA 146a Homo sapiens 33-41 29328400-5 2018 In HK-2 cells, overexpression of miR-146a inhibited Nox4 protein expression and decreased reactive oxygen species (ROS) generation, oxidative stress and inflammation, and suppressed vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) protein expression. Reactive Oxygen Species 115-118 microRNA 146a Homo sapiens 33-41 29328400-6 2018 Nacetylcysteine, a Nox4 inhibitor, was demonstrated to inhibit ROS generation, suppress VCAM-1 and ICAM-1 protein expression, and decrease oxidative stress and inflammation in HK-2 cells following overexpression of miR-146a. Acetylcysteine 0-15 microRNA 146a Homo sapiens 215-223 29328400-7 2018 In conclusion, these results indicated that miR-146a/Nox4 decreases ROS generation and inflammation and prevents DN. Reactive Oxygen Species 68-71 microRNA 146a Homo sapiens 44-52 29495389-7 2018 In the results, we showed that miR-146a-3p directly binds to and inhibits NIS. Nickel 74-77 microRNA 146a Homo sapiens 31-39 29495389-8 2018 Inhibition of miR-146a-3p restores the expression and function of NIS, increasing radioactive iodine uptake. Nickel 66-69 microRNA 146a Homo sapiens 14-22 29495389-8 2018 Inhibition of miR-146a-3p restores the expression and function of NIS, increasing radioactive iodine uptake. radioactive iodine 82-100 microRNA 146a Homo sapiens 14-22 29254567-6 2018 This simple AuNP-based CTG probing system, combined with isothermal amplification to induce a highly sensitive change in fluorescence, allows the detection of miRNA 146a with high sensitivity (14 aM) and selectivity. ctg 23-26 microRNA 146a Homo sapiens 159-169 29269299-8 2018 These findings suggest that the activation of TLR2 by bacterial components can enhance the progression of OSCC and may be implicated in acquired resistance to cisplatin-induced apoptosis through regulation of the miR-146a pathway. Cisplatin 159-168 microRNA 146a Homo sapiens 213-221 29357324-9 2018 Plasma TSH levels were positively correlated with miR-146a levels (r=0.321). Thyrotropin 7-10 microRNA 146a Homo sapiens 50-58 29357324-14 2018 Thus, miR-146a may have good predictive value for CHD among individuals with elevated TSH levels. Thyrotropin 86-89 microRNA 146a Homo sapiens 6-14 31966510-1 2017 The aim of this study is to explore the influence of miR-146a on cisplatin resistance in non-small cell lung cancer (NSCLC) cells and the related molecular mechanism. Cisplatin 65-74 microRNA 146a Homo sapiens 53-61 29292727-3 2017 In this study, we evaluated the effect of oxidative stress on miR-146a and miR-34a expression levels in human OA chondrocytes cultures stimulated by H2O2. Hydrogen Peroxide 149-153 microRNA 146a Homo sapiens 62-70 29292727-7 2017 Furthermore, H2O2 significantly up-regulated the expression levels of SOD-2, CAT, GPx and NRF2, and modulated miR-146a and miR-34a gene expression. Hydrogen Peroxide 13-17 microRNA 146a Homo sapiens 110-118 29292727-10 2017 Moreover, we demonstrated for the first time the modification of miR-146a and miR-34a in OA chondrocytes subjected to H2O2 stimulus and we confirmed the antioxidant effect of taurine. Hydrogen Peroxide 118-122 microRNA 146a Homo sapiens 65-73 31966510-6 2017 The expression of miR-146a in DDP-resistant NSCLC tumor samples was significantly lower than that in DDP-sensitive ones. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate 30-33 microRNA 146a Homo sapiens 18-26 31966510-6 2017 The expression of miR-146a in DDP-resistant NSCLC tumor samples was significantly lower than that in DDP-sensitive ones. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate 101-104 microRNA 146a Homo sapiens 18-26 31966510-11 2017 In conclusion, the study indicates that miR-146a regulates the DDP sensitivity by inhibiting NF-kappaB signaling pathway in NSCLC cells. 2-dimethylaminoethyl(dimethylamido)phosphonofluoridate 63-66 microRNA 146a Homo sapiens 40-48 29344219-0 2017 Upregulation of miR-146a increases cisplatin sensitivity of the non-small cell lung cancer A549 cell line by targeting JNK-2. Cisplatin 35-44 microRNA 146a Homo sapiens 16-24 29344219-1 2017 The aim of the present study was to investigate the effects of microRNA (miR-)146a on the cisplatin sensitivity of the non-small cell lung cancer (NSCLC) A549 cell line and study the underlying molecular mechanism. Cisplatin 90-99 microRNA 146a Homo sapiens 63-82 29344219-6 2017 The overexpression of miR-146a induced apoptosis and inhibited the growth and invasion of A549/DDP cells, which resulted in increased cisplatin sensitivity in NSCLC cells. Cisplatin 134-143 microRNA 146a Homo sapiens 22-30 29344219-9 2017 The upregulation of miR-146a increased cisplatin sensitivity of the A549 cell line by targeting JNK2, which may provide a novel method for treating NSCLC cisplatin resistance. Cisplatin 39-48 microRNA 146a Homo sapiens 20-28 29344219-9 2017 The upregulation of miR-146a increased cisplatin sensitivity of the A549 cell line by targeting JNK2, which may provide a novel method for treating NSCLC cisplatin resistance. Cisplatin 154-163 microRNA 146a Homo sapiens 20-28 28979106-8 2017 Diabetic patients showed more reduction in serum blood glucose than nondiabetics, with a great magnitude of reduction after the strength training intervention, which was paralleled by a positive change of the whole blood circulating levels of miR-146a, but not of the other miRs. Blood Glucose 49-62 microRNA 146a Homo sapiens 243-251 29108203-7 2017 A subgroup analysis of race, source of control population, and Hardy-Weinberg equilibrium were performed in these five genetic models, and miR-146a single nucleotide polymorphism increased the susceptibility to HCC only in the control population-based subgroups of the recessive model CG+GG/CC (OR = 1.20, 95% CI 1.02-1.40, P = 0.024). cysteinylglycine 285-287 microRNA 146a Homo sapiens 139-147 29049342-8 2017 A significant association was found between miR-146a rs2910164 polymorphisms and the risk of SCCHN in Chinese patients according to the overall data [CC+CG vs. GG: OR = 1.13; 95%CI = 1.00-1.29; CC vs. GG: OR = 1.19; 95%CI = 1.03-1.38]. cysteinylglycine 153-155 microRNA 146a Homo sapiens 44-52 28527151-6 2017 The CG/GG genotype of miR-146a rs2910164 tended to be associated with higher bronchial hyperresponsiveness to methacholine (PC20) compared with the CC genotype. Methacholine Chloride 110-122 microRNA 146a Homo sapiens 22-30 29037553-6 2017 RESULTS: Our results showed that there are significant differences in CG genotype frequencies between case and control groups regarding miR-146a rs2910164 polymorphism (OR = 2.03, CI = 1.3-3, P = 0.001). cysteinylglycine 70-72 microRNA 146a Homo sapiens 136-144 28433754-0 2017 miR-146a suppresses STAT3/VEGF pathways and reduces apoptosis through IL-6 signaling in primary human retinal microvascular endothelial cells in high glucose conditions. Glucose 150-157 microRNA 146a Homo sapiens 0-8 28433754-4 2017 The aim of this study was to investigate our hypothesis that miR-146a plays a role in suppressing pro-inflammatory pathways, involving STAT3 and VEGF, through regulating IL-6 signaling to reduce apoptosis of human retinal endothelial cells (REC) in high glucose conditions. Glucose 254-261 microRNA 146a Homo sapiens 61-69 28433754-7 2017 Overexpression of miR-146a reduced IL-6 levels, STAT3 phosphorylation, and VEGF levels in REC cultured in high glucose. Glucose 111-118 microRNA 146a Homo sapiens 18-26 28433754-10 2017 Overall, we report that miR-146a suppressed IL-6 signaling, leading to reduced levels of STAT3 and VEGF in REC in high glucose conditions, leading to decreased apoptosis. Glucose 119-126 microRNA 146a Homo sapiens 24-32 28927067-3 2017 miR-146a was evaluated in formalin-fixed, paraffin-embedded samples. Formaldehyde 26-34 microRNA 146a Homo sapiens 0-8 28927067-3 2017 miR-146a was evaluated in formalin-fixed, paraffin-embedded samples. Paraffin 42-50 microRNA 146a Homo sapiens 0-8 28927067-8 2017 Lower levels of miR-146a in primary tumor tissue samples were correlated with a shorter progression-free survival (P=0.04) and platinum-resistance of metastases (P=0.006). Platinum 127-135 microRNA 146a Homo sapiens 16-24 28783765-3 2017 Aminosulfonylarylisoxazole compounds exhibited higher specificity for miR-31 than for six other miRNAs, i.e., miR-15a, miR-16, miR-21, miR-92a-1, miR-146a, and miR-155, and increased the expression of miR-31 target genes. aminosulfonylarylisoxazole 0-26 microRNA 146a Homo sapiens 146-154 28573480-11 2017 As such, miRNA-146a may serve as a novel biomarker for the diagnosis of PSS, but not SLE. pss 72-75 microRNA 146a Homo sapiens 9-19 28748483-3 2017 MicroRNA-146a and microRNA-155 were detected by in situ hybridization with digoxigenin on paraffin sections. Digoxigenin 75-86 microRNA 146a Homo sapiens 0-13 28748483-3 2017 MicroRNA-146a and microRNA-155 were detected by in situ hybridization with digoxigenin on paraffin sections. Paraffin 90-98 microRNA 146a Homo sapiens 0-13 28454101-8 2017 MiR-146a mimics inhibited CaIG-induced activity of p-IkappaBalpha and translocation of NF-kappaB p65. caig 26-30 microRNA 146a Homo sapiens 0-8 28551628-0 2017 Regulation of miRNA-146a and miRNA-150 Levels by Celecoxib in Premalignant Lesions of K14-HPV16 Mice. Celecoxib 49-58 microRNA 146a Homo sapiens 14-24 28551628-7 2017 Celecoxib further increased miRNA-150 (p<0.05) and miRNA-146a levels in treated animals. Celecoxib 0-9 microRNA 146a Homo sapiens 54-64 28551628-9 2017 CONCLUSION: In this model, celecoxib may be able to regulate tumour-associated inflammation, through mechanisms involving the regulation of miRNA-146a and miRNA-150. Celecoxib 27-36 microRNA 146a Homo sapiens 140-150 28678319-0 2017 MiR-146a-5p level in serum exosomes predicts therapeutic effect of cisplatin in non-small cell lung cancer. Cisplatin 67-76 microRNA 146a Homo sapiens 0-8 28678319-3 2017 Our present study aimed to investigate the relation of the exosomal miR-146a-5p level with the chemosensitivity of NSCLC to cisplatin and the molecular mechanism that miR-146a-5p mediated to effect on chemotherapy response. Cisplatin 124-133 microRNA 146a Homo sapiens 68-76 28678319-11 2017 In the process of cisplatin-induced drug resistance, the expression of miR-146a-5p decreased in either NSCLC cell lines or the exosomes gradually. Cisplatin 18-27 microRNA 146a Homo sapiens 71-79 28678319-13 2017 And the possible mechanism of miR-146a-5p increasing chemosensitivity of NSCLC to cisplatin could be targeting Atg12 to inhibit autophagy. Cisplatin 82-91 microRNA 146a Homo sapiens 30-38 28678319-14 2017 CONCLUSIONS: Serum exosomal miR-146a-5p may be a new biomarker predicting the efficacy of cisplatin for NSCLC patients and real-time monitoring drug resistance. Cisplatin 90-99 microRNA 146a Homo sapiens 28-36 28324845-0 2017 Pharmacological effects of beta-d-mannuronic acid (M2000) on miR-146a, IRAK1, TRAF6 and NF-kappaB gene expression, as target molecules in inflammatory reactions. mannuronic acid 27-49 microRNA 146a Homo sapiens 61-69 28324845-3 2017 This research aimed to study the pharmaceutical effects of M2000 (beta-d-mannuronic acid) on the expression of miR-146a and its two target molecules (IRAK1 and TRAF6), and the transcription factor NF-kappaB in the HEK-Blue hTLR2 cell line. mannuronic acid 66-88 microRNA 146a Homo sapiens 111-119 28384720-5 2017 Results: The frequency of low copy numbers of miR-143, miR-146a, miR-9-3, and miR-205 and of high copy numbers of miR-301a and miR-23a was increased in patients with AAU+AS+ (P = 3.725 x 10-5 to 8.033 x 10-9). aau 166-169 microRNA 146a Homo sapiens 55-63 31994101-0 2017 Pharmacological effects of beta-D-mannuronic acid (M2000) on miR-146a, IRAK1, TRAF6 and NF-kappaB gene expression, as target molecules in inflammatory reactions. mannuronic acid 27-49 microRNA 146a Homo sapiens 61-69 31994101-3 2017 This research aimed to study the pharmaceutical effects of M2000 (beta-D-mannuronic acid) on the expression of miR-146a and its two target molecules (IRAK1 and TRAF6), and the transcription factor NF-kappaB in the HEK-Blue hTLR2 cell line. mannuronic acid 66-88 microRNA 146a Homo sapiens 111-119 27888401-7 2017 The influence of miR-146a inhibition on cholesterol expression in PBMCs was analysed in vitro after transient cell transfections with mirVana anti-miR-146a Inhibitor. Cholesterol 40-51 microRNA 146a Homo sapiens 17-25 27888401-10 2017 In vitro blockage of miR-146a expression in PBMCs of CHC patients greatly impaired intracellular cholesterol expression. Cholesterol 97-108 microRNA 146a Homo sapiens 21-29 27888401-11 2017 In these conditions, miR-146a expression was positively correlated with the intracellular cholesterol level. Cholesterol 90-101 microRNA 146a Homo sapiens 21-29 27888401-12 2017 These results suggest that genotype 1 HCV infection may alter miR-146a expression in PBMCs and, consequently, contribute to the observed dysregulation of cholesterol synthesis. Cholesterol 154-165 microRNA 146a Homo sapiens 62-70 28384720-10 2017 Conclusions: Low gene copy numbers of miR-143, miR-146a, miR-9-3, miR-205 and high gene copy numbers of miR-301a and miR-23a were associated with susceptibility to AAU+AS+. aau 164-167 microRNA 146a Homo sapiens 47-55 27706635-5 2016 Moreover, the CG+GG genotype of miR-146a was associated with an increased risk of ovarian cancer compared with the CC genotype (OR = 1.68, 95%CI = 1.06-2.66), and the GG genotype had a higher risk of ovarian cancer than the CC+CG genotype (OR = 3.02, 95%CI = 1.55-5.98). cysteinylglycine 14-16 microRNA 146a Homo sapiens 32-40 28119530-13 2017 In partial agreement, PA (but not HG) led to decreased miR-139-5p, miR-30b-5p, miR-422a and miR-146a in vitro, in parallel with increased lipogenesis and FA transport, decreased glucose metabolism and diminished FA oxidation. Palmitic Acid 22-24 microRNA 146a Homo sapiens 92-100 28218703-7 2017 Although the polyphenol-enriched fractions of blueberries could inhibit the microRNAs (miRNAs) (miR-21, miR-146a, and miR-125b) to different extents, no significant contribution from the PAs was observed. Polyphenols 13-23 microRNA 146a Homo sapiens 104-112 28337286-10 2017 Furthermore, the TGF-beta1 signaling inhibitor SB431542 impaired the ability of miR-146a knockdown to suppress LPS-induced angiogenesis. 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide 47-55 microRNA 146a Homo sapiens 80-88 28103112-0 2017 Potassium Iodate Differently Regulates the Proliferation, Migration, and Invasion of Human Thyroid Cancer Cells via Modulating miR-146a. potassium iodate 0-16 microRNA 146a Homo sapiens 127-135 28103112-2 2017 Results showed that the proliferation, migration, and invasion of SW579 thyroid cancer cells were improved by 10-6 M KIO3, which was associated with microRNA(miR)-146a deficit; 10-2 M KIO3 significantly enhanced miR-146a level and suppressed SW579 cell proliferation, migration, and invasion. kio3 117-121 microRNA 146a Homo sapiens 149-167 28103112-2 2017 Results showed that the proliferation, migration, and invasion of SW579 thyroid cancer cells were improved by 10-6 M KIO3, which was associated with microRNA(miR)-146a deficit; 10-2 M KIO3 significantly enhanced miR-146a level and suppressed SW579 cell proliferation, migration, and invasion. kio3 117-121 microRNA 146a Homo sapiens 212-220 28103112-2 2017 Results showed that the proliferation, migration, and invasion of SW579 thyroid cancer cells were improved by 10-6 M KIO3, which was associated with microRNA(miR)-146a deficit; 10-2 M KIO3 significantly enhanced miR-146a level and suppressed SW579 cell proliferation, migration, and invasion. kio3 184-188 microRNA 146a Homo sapiens 212-220 28103112-4 2017 Our study concludes that different doses of KIO3 have counteracting effects on the malignancy of thyroid cancer through modulating miR-146a level. kio3 44-48 microRNA 146a Homo sapiens 131-139 27998828-11 2017 Resveratrol and hydroxytyrosol 10muM induced NRf2 nuclear translocation and reduced miR-146a expression in LPS treated RAW 264.7. Resveratrol 0-11 microRNA 146a Homo sapiens 84-92 27998828-11 2017 Resveratrol and hydroxytyrosol 10muM induced NRf2 nuclear translocation and reduced miR-146a expression in LPS treated RAW 264.7. 3,4-dihydroxyphenylethanol 16-30 microRNA 146a Homo sapiens 84-92 27998828-12 2017 Overall, we reported an anti-inflammatory effect of resveratrol and hydroxytyrosol at low, nutritionally relevant concentrations, involving the inhibition of granulocytes and monocytes activation, the modulation of miR-146a expression and the activation of Nrf2. Resveratrol 52-63 microRNA 146a Homo sapiens 215-223 27998828-12 2017 Overall, we reported an anti-inflammatory effect of resveratrol and hydroxytyrosol at low, nutritionally relevant concentrations, involving the inhibition of granulocytes and monocytes activation, the modulation of miR-146a expression and the activation of Nrf2. 3,4-dihydroxyphenylethanol 68-82 microRNA 146a Homo sapiens 215-223 28101571-3 2017 In this study, gene set enrichment analysis (GSEA) showed negatively enriched expression of miR-146a target gene sets and positively enriched expression of gene sets suppressed by the enhancer of zeste homolog 2 (EZH2) after YY1 depletion in PCa cells. gsea 45-49 microRNA 146a Homo sapiens 92-100 27535005-9 2017 After MTX or topical treatment, reduction in PASI was observed [87.5% (75-100)]; miRNA-155 expression in PBMCs decreased; plasma miRNA-21, miRNA-146a and miRNA-223 were down-regulated. Methotrexate 6-9 microRNA 146a Homo sapiens 139-149 27913625-5 2017 miR-146a levels are also significantly reduced in the glomeruli of albuminuric BTBR ob/ob mice, indicating its significant role in maintaining podocyte health. btbr 79-83 microRNA 146a Homo sapiens 0-8 27901485-7 2017 The overall data indicated a significant association between miR-146a rs2910164 polymorphism and HNC risk [C vs. G: odds ratio (OR) = 1.14; 95% confidence interval (CI) = 1.00-1.31; CC+CG vs. GG: OR=1.21; 95%CI=1.02-1.43]. cysteinylglycine 185-187 microRNA 146a Homo sapiens 61-69 27562321-13 2016 CONCLUSION: We suggest that both miR-146a and miR-99a may serve as potential biomarkers for disease activity and clinical efficacy in psoriasis patients treated with ZG. Zg 166-168 microRNA 146a Homo sapiens 33-41 27802180-9 2016 The up-regulated miR-146a expression with agomir contributed to the differentiation of Th17 and Treg in ITP patients.Moreover, miR-146a was increased in the presence of DEX in PBMCs of ITP patients in vitro.Our study represents the abnormal expression profile of immune-related miRNAs in ITP patients, and miR-146a may be involved in Tregs differentiation and function. Dextromethorphan 169-172 microRNA 146a Homo sapiens 17-25 27802180-9 2016 The up-regulated miR-146a expression with agomir contributed to the differentiation of Th17 and Treg in ITP patients.Moreover, miR-146a was increased in the presence of DEX in PBMCs of ITP patients in vitro.Our study represents the abnormal expression profile of immune-related miRNAs in ITP patients, and miR-146a may be involved in Tregs differentiation and function. Dextromethorphan 169-172 microRNA 146a Homo sapiens 127-135 27802180-9 2016 The up-regulated miR-146a expression with agomir contributed to the differentiation of Th17 and Treg in ITP patients.Moreover, miR-146a was increased in the presence of DEX in PBMCs of ITP patients in vitro.Our study represents the abnormal expression profile of immune-related miRNAs in ITP patients, and miR-146a may be involved in Tregs differentiation and function. Dextromethorphan 169-172 microRNA 146a Homo sapiens 127-135 27904770-2 2016 Our results showed that miR-146a was significantly downregulated in drug-resistant K562 cells and the overexpression of miR-146a in K562/ADM cells could restore the sensitivity to adriamycin (ADM). Doxorubicin 180-190 microRNA 146a Homo sapiens 24-32 27904770-2 2016 Our results showed that miR-146a was significantly downregulated in drug-resistant K562 cells and the overexpression of miR-146a in K562/ADM cells could restore the sensitivity to adriamycin (ADM). Doxorubicin 180-190 microRNA 146a Homo sapiens 120-128 27904770-2 2016 Our results showed that miR-146a was significantly downregulated in drug-resistant K562 cells and the overexpression of miR-146a in K562/ADM cells could restore the sensitivity to adriamycin (ADM). Doxorubicin 137-140 microRNA 146a Homo sapiens 24-32 27904770-2 2016 Our results showed that miR-146a was significantly downregulated in drug-resistant K562 cells and the overexpression of miR-146a in K562/ADM cells could restore the sensitivity to adriamycin (ADM). Doxorubicin 137-140 microRNA 146a Homo sapiens 120-128 27449900-6 2016 Here, we aimed to investigate the role of miR-146a and its possible target genes in human SK-N-SH cells subjected to 16h of oxygen-glucose deprivation and 12h of reperfusion (OGD/R) injury. Oxygen 124-130 microRNA 146a Homo sapiens 42-50 27449900-6 2016 Here, we aimed to investigate the role of miR-146a and its possible target genes in human SK-N-SH cells subjected to 16h of oxygen-glucose deprivation and 12h of reperfusion (OGD/R) injury. Glucose 131-138 microRNA 146a Homo sapiens 42-50 27569893-3 2016 The luciferase reporter gene technique was adopted to verify that MIF was the specific reverse target gene of miR-146a and the liposome Lipofectamine 2000 was employed to transfer the modeled miR-146a mimics, and miR-146a negative control (NC) in NSCLC cells to detect the expression of MIF mRNA and protein. Lipofectamine 136-154 microRNA 146a Homo sapiens 192-200 27569893-3 2016 The luciferase reporter gene technique was adopted to verify that MIF was the specific reverse target gene of miR-146a and the liposome Lipofectamine 2000 was employed to transfer the modeled miR-146a mimics, and miR-146a negative control (NC) in NSCLC cells to detect the expression of MIF mRNA and protein. Lipofectamine 136-154 microRNA 146a Homo sapiens 192-200 26916895-8 2016 RESULTS: The miR-146a component was found to be downregulated in glioma tissue compared with adjacent nontumor tissue (p&lt;0.05). Adenosine Monophosphate 121-124 microRNA 146a Homo sapiens 13-21 27269729-4 2016 In this study, PF6 was shown to form unimodal nanocomplexes with miR-146a mimic that entered into human primary keratinocytes, where miR-146a inhibited the expression of its direct targets from the NF-kappaB pathway and the genes known to be activated by NF-kappaB, C-C motif ligand (CCL)5 and interleukin (IL)-8. pf6 15-18 microRNA 146a Homo sapiens 65-73 27269729-4 2016 In this study, PF6 was shown to form unimodal nanocomplexes with miR-146a mimic that entered into human primary keratinocytes, where miR-146a inhibited the expression of its direct targets from the NF-kappaB pathway and the genes known to be activated by NF-kappaB, C-C motif ligand (CCL)5 and interleukin (IL)-8. pf6 15-18 microRNA 146a Homo sapiens 133-141 27463381-7 2016 Chitin induced the expression of miR-155, miR-146a and miR-21, each of which is known to up-regulate the expression of pro-inflammatory cytokines. Chitin 0-6 microRNA 146a Homo sapiens 42-50 27351285-7 2016 miR146a-induced downregulation of FANCM was associated with inhibition of FANCD2 monoubiquitination, reduced DNA homologous recombination repair and checkpoint response, failed recovery from replication stress, and increased cellular sensitivity to cisplatin. Cisplatin 249-258 microRNA 146a Homo sapiens 0-7 27163405-0 2016 Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-kappaB activation. Orthosilicic acid 0-17 microRNA 146a Homo sapiens 91-99 27163405-0 2016 Orthosilicic acid, Si(OH)4, stimulates osteoblast differentiation in vitro by upregulating miR-146a to antagonize NF-kappaB activation. si(oh)4 19-26 microRNA 146a Homo sapiens 91-99 27163405-4 2016 To elucidate the possible molecular mechanisms, differential microRNA microarray analysis was used to show that Si(OH)4 significantly up-regulated microRNA-146a (miR-146a) expression during hMSC osteogenic differentiation. si(oh)4 112-119 microRNA 146a Homo sapiens 147-160 27163405-4 2016 To elucidate the possible molecular mechanisms, differential microRNA microarray analysis was used to show that Si(OH)4 significantly up-regulated microRNA-146a (miR-146a) expression during hMSC osteogenic differentiation. si(oh)4 112-119 microRNA 146a Homo sapiens 162-170 27163405-5 2016 Si(OH)4 induced miR-146a expression profiling was further validated by quantitative RT-PCR (qRT-PCR), which indicated miR-146a was up-regulated during the late stages of hMSC osteogenic differentiation. si(oh)4 0-7 microRNA 146a Homo sapiens 16-24 27163405-5 2016 Si(OH)4 induced miR-146a expression profiling was further validated by quantitative RT-PCR (qRT-PCR), which indicated miR-146a was up-regulated during the late stages of hMSC osteogenic differentiation. si(oh)4 0-7 microRNA 146a Homo sapiens 118-126 27163405-7 2016 Furthermore, luciferase reporter assay, Western blotting, enzyme-linked immunosorbent assay (ELISA), and immunofluorescence showed that Si(OH)4 decreased TNFalpha-induced activation of NF-kappaB, a signal transduction pathway that inhibits osteoblastic bone formation, through the known miR-146a negative feedback loop. si(oh)4 136-143 microRNA 146a Homo sapiens 287-295 27163405-8 2016 Our studies established a mechanism for Si(OH)4 to promote osteogenesis by antagonizing NF-kappaB activation via miR-146a, which might be interesting to guide the design of osteo-inductive biomaterials for treatments of bone defects in humans. si(oh)4 40-47 microRNA 146a Homo sapiens 113-121 27163405-12 2016 We identified that miR-146a is the expression signature in bone cells treated with Si(OH)4. si(oh)4 83-90 microRNA 146a Homo sapiens 19-27 27163405-13 2016 Further analysis of miR-146a in bone cells reveals that Si(OH)4 upregulates miR-146a to antagonize the activation of NF-kappaB. si(oh)4 56-63 microRNA 146a Homo sapiens 20-28 27163405-13 2016 Further analysis of miR-146a in bone cells reveals that Si(OH)4 upregulates miR-146a to antagonize the activation of NF-kappaB. si(oh)4 56-63 microRNA 146a Homo sapiens 76-84 27102001-6 2016 DAPT, an inhibitor of the endogenous Notch pathway, was able to abrogate the miR-146a-induced increase of cytokines in MSC, suggesting the involvement of the Notch pathway. dapt 0-4 microRNA 146a Homo sapiens 77-85 27093470-10 2016 The modifying effect of rs2910164 on the PAHs-HRV associations suggested miR-146a may mediate the effects of PAH exposure on HRV. Polycyclic Aromatic Hydrocarbons 41-44 microRNA 146a Homo sapiens 73-81 27079198-0 2016 Expression of miR-146a, miR-155, and miR-223 in formalin-fixed paraffin-embedded synovial tissues of patients with rheumatoid arthritis and osteoarthritis. Formaldehyde 48-56 microRNA 146a Homo sapiens 14-22 26429200-8 2016 Changes in miR-192, miR-146a, miR-148a, miR-15a, and miR-21 were positively correlated (p<0.05) with alanine aminotransferase in simvastatin-only treated patients. Simvastatin 132-143 microRNA 146a Homo sapiens 20-28 27158964-6 2016 As the miR-146a increased, the probability of suffering from silicosis increased for stage I patients, and for stage II & III patients, the probability first increased and then decreased. Adenosine Monophosphate 121-124 microRNA 146a Homo sapiens 7-15 25727911-0 2016 Downregulation of miR-146a, cyclooxygenase-2 and advanced glycation end-products in simvastatin-treated older patients with hyperlipidemia. Simvastatin 84-95 microRNA 146a Homo sapiens 18-26 30090394-0 2016 MiR-146a affects the alteration in myeloid differentiation induced by hydroquinone in human CD34+ hematopoietic progenitor cells and HL-60 cells. hydroquinone 70-82 microRNA 146a Homo sapiens 0-8 30090394-5 2016 Using the miR-146a-5p inhibitor to suppress miR-146a expression could relieve the inhibitory effect on myeloid differentiation induced by hydroquinone to a certain extent. hydroquinone 138-150 microRNA 146a Homo sapiens 10-18 30090394-5 2016 Using the miR-146a-5p inhibitor to suppress miR-146a expression could relieve the inhibitory effect on myeloid differentiation induced by hydroquinone to a certain extent. hydroquinone 138-150 microRNA 146a Homo sapiens 44-52 30090394-7 2016 These results suggested that hydroquinone induced a dysregulation of miR-146a and its downstream NF-kappaB transcriptional factor pathway, which might be an early event in the generation of benzene-induced differentiation disturbance and subsequent leukemogenesis. hydroquinone 29-41 microRNA 146a Homo sapiens 69-77 30090394-7 2016 These results suggested that hydroquinone induced a dysregulation of miR-146a and its downstream NF-kappaB transcriptional factor pathway, which might be an early event in the generation of benzene-induced differentiation disturbance and subsequent leukemogenesis. Benzene 190-197 microRNA 146a Homo sapiens 69-77 26827637-7 2016 Moreover, sulforaphane significantly attenuated the levels of microRNA-146a, which is selectively upregulated in the temporal cortex and hippocampus of AD brains. sulforaphane 10-22 microRNA 146a Homo sapiens 62-75 26827637-9 2016 These results indicate that signal transducer and activator of transcription-1 dephosphorylation, HO-1 and its upstream effector, Nrf2, play a pivotal role in triggering an anti-inflammatory signaling cascade of sulforaphane that results in decreases of IL-1beta release and microRNA-146a production in Abeta1-42-stimulated human microglia-like cells. sulforaphane 212-224 microRNA 146a Homo sapiens 275-288 27131313-7 2016 Overexpression of miR-146a increased the reactive oxygen species (ROS) level and decreased SOD2 mRNA and protein expression. Reactive Oxygen Species 41-64 microRNA 146a Homo sapiens 18-26 27057540-5 2016 METHODS: To explore the effect of miR-146a/bFGF on inflammation and tissue regeneration, polyethylene glycol-polyethyleneimine (PEG-PEI) was synthesized, and physical characteristics were analyzed by dynamic light scattering and gel retardation analysis. polyethylene glycol-polyethyleneimine 89-126 microRNA 146a Homo sapiens 34-42 27057540-7 2016 Alginate gel was combined with miR-146a/PEG-PEI nanoparticles and bFGF. Alginates 0-8 microRNA 146a Homo sapiens 31-39 27131313-7 2016 Overexpression of miR-146a increased the reactive oxygen species (ROS) level and decreased SOD2 mRNA and protein expression. Reactive Oxygen Species 66-69 microRNA 146a Homo sapiens 18-26 27131313-11 2016 miR-146a downregulates the expression of SOD2 and enhances ROS generation, leading to increased apoptosis, inhibition of proliferation, and enhanced sensitivity to chemotherapy. Reactive Oxygen Species 59-62 microRNA 146a Homo sapiens 0-8 27131313-12 2016 The data demonstrate that the miR-146a/SOD2/ROS pathway may serve as a novel therapeutic target and prognostic marker in patients with EOC. Reactive Oxygen Species 44-47 microRNA 146a Homo sapiens 30-38 25957028-7 2015 TRAF6 siRNA or JNK inhibitor SP600125 significantly reduced LPS-induced miR-146a-5p increase in astrocytes. pyrazolanthrone 29-37 microRNA 146a Homo sapiens 72-80 26997759-0 2016 miR-146a Attenuates Inflammatory Pathways Mediated by TLR4/NF-kappaB and TNFalpha to Protect Primary Human Retinal Microvascular Endothelial Cells Grown in High Glucose. Glucose 161-168 microRNA 146a Homo sapiens 0-8 26997759-7 2016 Our results demonstrate that miR-146a expression was decreased in human REC cultured in high glucose. Glucose 93-100 microRNA 146a Homo sapiens 29-37 26997759-8 2016 Overexpression of miR-146a using mimics reduced the levels of TLR4/NF-kappaB and TNFalpha in REC cultured in high glucose. Glucose 114-121 microRNA 146a Homo sapiens 18-26 26997759-9 2016 Both MyD88-dependent and -independent signaling were decreased by miR-146a overexpression in REC in high glucose conditions. Glucose 105-112 microRNA 146a Homo sapiens 66-74 26306811-4 2015 Moreover, the impact of miR-146a on prostate cancer cells apoptosis were detected by Hoechst staining and fluorescence-activated cell sorter (FACS). hoechst 85-92 microRNA 146a Homo sapiens 24-32 26862480-7 2016 RESULTS: For the rs2910164 polymorphism of miR-146a, significantly increased risks for HCC were observed when all studies were pooled under two models (CG vs CC: OR = 1.11, 95% CI = 1.02-1.21, P = 0.021; GG + CG vs CC: OR = 1.11, 95% CI = 1.01-1.22, P = 0.035). cysteinylglycine 152-154 microRNA 146a Homo sapiens 43-51 26862480-7 2016 RESULTS: For the rs2910164 polymorphism of miR-146a, significantly increased risks for HCC were observed when all studies were pooled under two models (CG vs CC: OR = 1.11, 95% CI = 1.02-1.21, P = 0.021; GG + CG vs CC: OR = 1.11, 95% CI = 1.01-1.22, P = 0.035). cysteinylglycine 209-211 microRNA 146a Homo sapiens 43-51 26239619-2 2015 The present study was undertaken to determine whether the cytotoxicity of curcumin (diferuloylmethane), a natural polyphenolic compound isolated from turmeric (Curcuma longa Linn), in glioblastoma cells is mediated through upregulation of miR-146a. Curcumin 84-101 microRNA 146a Homo sapiens 239-247 26239619-5 2015 Curcumin exposure led to upregulation of miR-146a in U-87 MG cells. Curcumin 0-8 microRNA 146a Homo sapiens 41-49 26239619-7 2015 Notably, curcumin-mediated enhancement of TMZ-induced apoptosis was blocked by depletion of miR-146a. Curcumin 9-17 microRNA 146a Homo sapiens 92-100 26239619-7 2015 Notably, curcumin-mediated enhancement of TMZ-induced apoptosis was blocked by depletion of miR-146a. Temozolomide 42-45 microRNA 146a Homo sapiens 92-100 26239619-8 2015 By contrast, miR-146a overexpression enhanced apoptosis and suppressed NF-kappaB activation in TMZ-treated cells. Temozolomide 95-98 microRNA 146a Homo sapiens 13-21 26239619-10 2015 To the best of our knowledge, the present study provides the first evidence that upregulation of miR-146a and inactivation of NF-kappaB signaling mediates the sensitization of human glioblastoma cells to TMZ-induced apoptosis by curcumin. Temozolomide 204-207 microRNA 146a Homo sapiens 97-105 26239619-10 2015 To the best of our knowledge, the present study provides the first evidence that upregulation of miR-146a and inactivation of NF-kappaB signaling mediates the sensitization of human glioblastoma cells to TMZ-induced apoptosis by curcumin. Curcumin 229-237 microRNA 146a Homo sapiens 97-105 26396533-0 2015 Polymorphism in miR-146a associated with clinical characteristics and outcomes in gastric cancer patients treated with adjuvant oxaliplatin and fluoropyrimidines. Oxaliplatin 128-139 microRNA 146a Homo sapiens 16-24 26396533-0 2015 Polymorphism in miR-146a associated with clinical characteristics and outcomes in gastric cancer patients treated with adjuvant oxaliplatin and fluoropyrimidines. fluoropyrimidines 144-161 microRNA 146a Homo sapiens 16-24 26224317-6 2015 In addition, the suppression of histone deacetylase (HDAC) activities by trichostatin A improved miR-146a expression due to the up-regulation of the DNA-binding activity of NF-kappaB at the miR-146a promoter in TRAIL-induced macrophages, suggesting that histone acetylation was involved in the suppression of miR-146a expression. trichostatin A 73-87 microRNA 146a Homo sapiens 97-105 26224317-6 2015 In addition, the suppression of histone deacetylase (HDAC) activities by trichostatin A improved miR-146a expression due to the up-regulation of the DNA-binding activity of NF-kappaB at the miR-146a promoter in TRAIL-induced macrophages, suggesting that histone acetylation was involved in the suppression of miR-146a expression. trichostatin A 73-87 microRNA 146a Homo sapiens 190-198 26224317-6 2015 In addition, the suppression of histone deacetylase (HDAC) activities by trichostatin A improved miR-146a expression due to the up-regulation of the DNA-binding activity of NF-kappaB at the miR-146a promoter in TRAIL-induced macrophages, suggesting that histone acetylation was involved in the suppression of miR-146a expression. trichostatin A 73-87 microRNA 146a Homo sapiens 190-198 26345457-8 2015 RESULTS: We found that miR-146a was significant overexpressed and correlated significantly with BPA accumulation in the placenta from pregnant women living in a polluted area and undergoing therapeutic abortion due to fetal malformations. bisphenol A 96-99 microRNA 146a Homo sapiens 23-31 26345457-10 2015 CONCLUSIONS: For the first time, we found, in humans, that miR-146a was significant over-expressed and correlated significantly with BPA accumulation in the placenta. bisphenol A 133-136 microRNA 146a Homo sapiens 59-67 25661834-0 2015 Mycophenolic acid upregulates miR-142-3P/5P and miR-146a in lupus CD4+T cells. Mycophenolic Acid 0-17 microRNA 146a Homo sapiens 48-56 25877355-3 2015 After treated by interferon/ribavirin, miR-146a expression was decreased when HCV RNA became undetectable. Ribavirin 28-37 microRNA 146a Homo sapiens 39-47 25873300-10 2015 The current findings demonstrated that beta2-AR signaling has growth inhibitory effects via modulation of the cAMP/PKA pathway in A-1321N1 cells through increasing the expression level of Cx43 and miR-146a as well as decreasing miR-155 and miR-27a levels. Cyclic AMP 110-114 microRNA 146a Homo sapiens 197-205 25596948-0 2015 Quercetin inhibits proliferation and invasion acts by up-regulating miR-146a in human breast cancer cells. Quercetin 0-9 microRNA 146a Homo sapiens 68-76 25596948-6 2015 All the results demonstrated that quercetin exhibited excellent effect on inhibiting cell proliferation in human breast cancer cells, which was performed by up-regulating miR-146a expression, then via inducing apoptosis through caspase-3 activation and mitochondrial-dependent pathways, and inhibiting invasion through down-regulating the expression of EGFR. Quercetin 34-43 microRNA 146a Homo sapiens 171-179 25767384-6 2015 We observed a significant association between rs2910164 in miR-146a and the levels of either COX2 or PGE2 using real-time polymerase chain reaction and Western blot. Dinoprostone 101-105 microRNA 146a Homo sapiens 59-67 24796653-12 2015 Interestingly, decreased miR-146a expression was significantly associated with high serum GADA titers (P < 0.05). gada 90-94 microRNA 146a Homo sapiens 25-33 25608619-7 2015 DNA methylation status of miR-146a promoter were performed by PCR analysis of bisulfite-modified genomic DNA. hydrogen sulfite 78-87 microRNA 146a Homo sapiens 26-34 25951497-10 2015 Upregulation of miR-21 and miR-146a was also detected in formalin-fixed, paraffin-embedded UM, suggesting that VH or serum alterations in UM could be the consequence of disregulation arising from tumoral cells. Formaldehyde 57-65 microRNA 146a Homo sapiens 27-35 25951497-10 2015 Upregulation of miR-21 and miR-146a was also detected in formalin-fixed, paraffin-embedded UM, suggesting that VH or serum alterations in UM could be the consequence of disregulation arising from tumoral cells. Paraffin 73-81 microRNA 146a Homo sapiens 27-35 26604920-4 2015 To find out whether NB-UVB or methotrexate treatment affects whole blood levels of human miRNA (146a) in patients with psoriasis and demonstrate its correlation with disease severity. Methotrexate 30-42 microRNA 146a Homo sapiens 89-100 26604920-10 2015 Real Time PCR showed that, after 12 weeks of treatment with NB-UVB phototherapy or treatment with methotrexate, there was significantly decreased level of miR146a (P = 0.001; P = 0.002, resp.). Methotrexate 98-110 microRNA 146a Homo sapiens 155-162 25008481-12 2014 Our study established MIR146A rs2431697 as a prognostic biomarker for ACE in anticoagulated AF patients. Acetaldehyde 70-73 microRNA 146a Homo sapiens 22-29 25546664-8 2014 With respect to miR-146a rs2910164 polymorphism, statistical significant increased HCC risk was found when all studies were pooled into the meta-analysis (GG+CG vs CC: OR = 1.097, 95% CI 1.005-1.197, P = 0.037). cysteinylglycine 158-160 microRNA 146a Homo sapiens 16-24 25052989-7 2014 This is because miR-146a inhibitor abrogated the inhibitory effects of denbinobin. denbinobin 71-81 microRNA 146a Homo sapiens 16-24 24952884-5 2014 In subgroup meta-analysis, rs2910164 in miR-146a and large-artery atherosclerosis, rather than small-vessel disease, showed the significant association under the dominant model (CC vs CG+GG, OR 1.694; 95 % CI 1.199-2.395 p = 0.003). cysteinylglycine 184-186 microRNA 146a Homo sapiens 40-48 25182190-5 2014 RESULTS: The expression of both miR-155 and miR-146a was increased more than fivefold in the kidney samples of the DN patients compared with the controls, and the miR-155 expression was closely correlated with the serum creatinine levels (R = 0.95, P = 0.004). Creatinine 220-230 microRNA 146a Homo sapiens 44-52 25182190-7 2014 In vitro, high glucose induced the over-expression of miR-155 and miR-146a in the HRGECs, which, in turn, increased the TNF-alpha, TGF-beta1, and NF-kappaB expression. Glucose 15-22 microRNA 146a Homo sapiens 66-74 25183503-4 2014 Our studies showed that exposure to PD98059, TPCA-1 and LY294002 resulted in a dose-dependent reduction in the expression of mature miR-146a while the primary miR-146a expression was not changed by any inhibitor. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 36-43 microRNA 146a Homo sapiens 132-140 25183503-4 2014 Our studies showed that exposure to PD98059, TPCA-1 and LY294002 resulted in a dose-dependent reduction in the expression of mature miR-146a while the primary miR-146a expression was not changed by any inhibitor. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 36-43 microRNA 146a Homo sapiens 159-167 25183503-4 2014 Our studies showed that exposure to PD98059, TPCA-1 and LY294002 resulted in a dose-dependent reduction in the expression of mature miR-146a while the primary miR-146a expression was not changed by any inhibitor. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 56-64 microRNA 146a Homo sapiens 132-140 25183503-4 2014 Our studies showed that exposure to PD98059, TPCA-1 and LY294002 resulted in a dose-dependent reduction in the expression of mature miR-146a while the primary miR-146a expression was not changed by any inhibitor. 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one 56-64 microRNA 146a Homo sapiens 159-167 24908639-6 2014 The expression of platelet miR-223 and miR-146a significantly correlated with plasma miR-223 and miR-146a levels, blood glucose concentration, and platelet activation rate. Glucose 120-127 microRNA 146a Homo sapiens 39-47 24839931-4 2014 Treatment of PC cells with CDF, a novel synthetic compound, led to re-expression of miR-146a, resulting in the down-regulation of EGFR expression. CAF protocol 27-30 microRNA 146a Homo sapiens 84-92 24839931-8 2014 Collectively, these results suggest that the loss of expression of miR-146a is a fundamental mechanism for over-expression of EGFR signaling and that re-expression of miR-146a by CDF treatment could be useful in designing personalized strategy for the treatment of human PC. CAF protocol 179-182 microRNA 146a Homo sapiens 167-175 24740563-6 2014 Association between miR-146a rs2910164 polymorphism and risk of colorectal cancer was detected with effect modification by alcohol drinking status (P for interaction = 0.010). Alcohols 123-130 microRNA 146a Homo sapiens 20-28 25047043-9 2014 Introduction of miR-146a can specifically ablate COX-2 protein and the biological activity of COX-2 as measured by prostaglandin production. Prostaglandins 115-128 microRNA 146a Homo sapiens 16-24 24863965-2 2014 We demonstrated that lipopolysaccharide (LPS) induced the upregulation of miR-146a in human umbilical vein endothelial cells (HUVECs), and that the induction was blocked by silencing toll-like receptors, the adaptor molecule MyD88, and the nonspecific NF-kappaB inhibitor BAY 11-7082. 3-(4-methylphenylsulfonyl)-2-propenenitrile 272-283 microRNA 146a Homo sapiens 74-82 24630744-0 2014 A genetic variant in the microRNA-146a gene is associated with susceptibility to alcohol use disorders. Alcohols 81-88 microRNA 146a Homo sapiens 25-38 24885368-0 2014 Demethylation of the miR-146a promoter by 5-Aza-2"-deoxycytidine correlates with delayed progression of castration-resistant prostate cancer. Decitabine 42-64 microRNA 146a Homo sapiens 21-29 24885368-6 2014 The methylation levels of miR-146a promoter region in the different groups were quantified by the bisulfite sequencing PCR (BSP) assay. hydrogen sulfite 98-107 microRNA 146a Homo sapiens 26-34 24670457-3 2014 MTT essay was used to evaluate the proliferation of colonic cancer SW260 cells transfected with miR-146a mimics, and the cell cycle and apoptosis of the cells were analyzed with flow cytometry. monooxyethylene trimethylolpropane tristearate 0-3 microRNA 146a Homo sapiens 96-104 24172202-3 2014 OBJECTIVE: To explore the clinicopathological significance of the miR-146a level in HCC formalin-fixed paraffin-embedded (FFPE) tissue. Formaldehyde 88-96 microRNA 146a Homo sapiens 66-74 24172202-3 2014 OBJECTIVE: To explore the clinicopathological significance of the miR-146a level in HCC formalin-fixed paraffin-embedded (FFPE) tissue. Paraffin 103-111 microRNA 146a Homo sapiens 66-74 24334435-8 2014 OECs from T1D participants are TLR-hyper-responsive, due to dysregulated induction of miR146a and miR155, which is abrogated by pre-treatment with triclosan. Triclosan 147-156 microRNA 146a Homo sapiens 86-93 23953512-3 2014 Cyclooxygenase 2 - the key enzyme of the prostanoid pathway - is regulated by different miRNAs such as miRNA-101, miR199a, miR26b and miR-146a. Prostaglandins 41-51 microRNA 146a Homo sapiens 134-142 23953512-3 2014 Cyclooxygenase 2 - the key enzyme of the prostanoid pathway - is regulated by different miRNAs such as miRNA-101, miR199a, miR26b and miR-146a. mirna-101 103-112 microRNA 146a Homo sapiens 134-142 24895573-1 2014 Previously, we found that the expression of microRNA-146a (miR-146a) was downregulated in hepatocellular carcinoma (HCC) formalin-fixed paraffin-embedded (FFPE) tissues compared to the adjacent noncancerous hepatic tissues. Formaldehyde 121-129 microRNA 146a Homo sapiens 44-57 24895573-1 2014 Previously, we found that the expression of microRNA-146a (miR-146a) was downregulated in hepatocellular carcinoma (HCC) formalin-fixed paraffin-embedded (FFPE) tissues compared to the adjacent noncancerous hepatic tissues. Formaldehyde 121-129 microRNA 146a Homo sapiens 59-67 24895573-1 2014 Previously, we found that the expression of microRNA-146a (miR-146a) was downregulated in hepatocellular carcinoma (HCC) formalin-fixed paraffin-embedded (FFPE) tissues compared to the adjacent noncancerous hepatic tissues. Paraffin 136-144 microRNA 146a Homo sapiens 44-57 24895573-1 2014 Previously, we found that the expression of microRNA-146a (miR-146a) was downregulated in hepatocellular carcinoma (HCC) formalin-fixed paraffin-embedded (FFPE) tissues compared to the adjacent noncancerous hepatic tissues. Paraffin 136-144 microRNA 146a Homo sapiens 59-67 24802714-9 2014 In addition, logistic binary regression analyses show miR-222 is positively associated with serum insulin, while miR-146a is negatively associated with serum testosterone. Testosterone 158-170 microRNA 146a Homo sapiens 113-121 25298619-10 2014 In contrast, miR-146a mimic transfection attenuated HG/thrombin-induced upregulation of Nox4 expression, ROS generation, and inflammatory phenotypes. ros 105-108 microRNA 146a Homo sapiens 13-21 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Vorinostat 17-21 microRNA 146a Homo sapiens 105-113 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Vorinostat 17-21 microRNA 146a Homo sapiens 196-204 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Vorinostat 23-33 microRNA 146a Homo sapiens 105-113 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Vorinostat 23-33 microRNA 146a Homo sapiens 196-204 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 microRNA 146a Homo sapiens 105-113 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 40-46 microRNA 146a Homo sapiens 196-204 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 microRNA 146a Homo sapiens 105-113 24107356-8 2013 HDAC inhibitors, SAHA (vorinostat), and LBH589 (panobinostat) significantly (6.1- and 5.4-fold) elevated miR-146a expression by increasing the binding of the transcription factor NF-kappaB to the miR-146a promoter, and negatively regulated IL-1beta-induced IKK/IkappaB/p65 phosphorylation signaling and IL-6 secretion. Panobinostat 48-60 microRNA 146a Homo sapiens 196-204 23564509-12 2013 miR-146a overexpression ablated the effects of RelB downregulation on IL-1beta-induced Cox-2, PGE2, and IL-6 production, suggesting that RelB mediates IL-1beta-induced inflammatory mediator production in lung fibroblasts through miRNA-146a. Dinoprostone 94-98 microRNA 146a Homo sapiens 0-8 24030097-0 2013 Time dependence of cisplatin-induced duplex dissociation of 15-mer RNAs and mature miR-146a. Cisplatin 19-28 microRNA 146a Homo sapiens 83-91 24030097-1 2013 The kinetics for the binding of cisplatin to duplex RNAs, two fully complementary model systems and mature miR-146a, exhibits a linear dependence on cisplatin concentration and results in duplex dissociation at 38 C. Cisplatin 32-41 microRNA 146a Homo sapiens 107-115 24030097-1 2013 The kinetics for the binding of cisplatin to duplex RNAs, two fully complementary model systems and mature miR-146a, exhibits a linear dependence on cisplatin concentration and results in duplex dissociation at 38 C. Cisplatin 149-158 microRNA 146a Homo sapiens 107-115 23727324-0 2013 Anti-inflammatory effect of ubiquinol-10 on young and senescent endothelial cells via miR-146a modulation. ubiquinol-10 28-40 microRNA 146a Homo sapiens 86-94 23898084-7 2013 Moreover, a multivariate analysis showed that the CC genotype of miR-146a rs2910164 was associated with worse relapse-free and disease-specific survival compared to the CG or GG genotype in a recessive model of the C allele, adjusted for patient and tumor characteristics (hazard ratio=2.120 and 2.349, p=0.005 and 0.007, respectively). cysteinylglycine 169-171 microRNA 146a Homo sapiens 65-73 23812247-8 2013 Increased serum levels of Cathepsin D, the enzyme that generates 16 kDa Prolactin, miR-146a, a direct target of 16 kDa Prolactin, N-terminal-pro-brain-natriuretic peptide (NT-proBNP) and asymmetric dimethylarginine (ADMA) emerged as biomarkers for PPCM. dimethylarginine 198-214 microRNA 146a Homo sapiens 83-91 23812247-8 2013 Increased serum levels of Cathepsin D, the enzyme that generates 16 kDa Prolactin, miR-146a, a direct target of 16 kDa Prolactin, N-terminal-pro-brain-natriuretic peptide (NT-proBNP) and asymmetric dimethylarginine (ADMA) emerged as biomarkers for PPCM. N,N-dimethylarginine 216-220 microRNA 146a Homo sapiens 83-91 23616185-7 2013 Additionally, we detected an altered distribution of miR-155 and miR-146a expression related with HbA1c, glucose and BMI using the analysis of a three dimensional association of variables in the group of T2D patients.Downregulated levels of miR-155 could play an important role in the pathogenesis of T2D due to their relationship with metabolic control. Glucose 105-112 microRNA 146a Homo sapiens 65-73 23459235-5 2013 We identified seven microRNAs (miR-124a, miR-146a &amp; b, miR-185, miR-16 and let-7a &amp; b), which displayed significant differential expression in normal prostate tissue from men with prostate cancer compared to both cancer negative control groups. Adenosine Monophosphate 51-54 microRNA 146a Homo sapiens 41-49 23706078-0 2013 Celastrol induces apoptosis of gastric cancer cells by miR-146a inhibition of NF-kappaB activity. celastrol 0-9 microRNA 146a Homo sapiens 55-63 23706078-5 2013 Finally, the effect of miR-146a on celastrol-induced anti-tumor activity was assessed using miR-146a inhibitor. celastrol 35-44 microRNA 146a Homo sapiens 23-31 23706078-5 2013 Finally, the effect of miR-146a on celastrol-induced anti-tumor activity was assessed using miR-146a inhibitor. celastrol 35-44 microRNA 146a Homo sapiens 92-100 23706078-8 2013 Furthermore, Celastrol could increase miR-146a expression and up-regulation of miR-146a expression could suppress NF-kappaB activity. celastrol 13-22 microRNA 146a Homo sapiens 38-46 23706078-9 2013 More important, down-regulation of miR-146a expression can reverse the effect of celastrol on NF-kappaB activity and apoptosis in gastric cancer cells. celastrol 81-90 microRNA 146a Homo sapiens 35-43 23706078-10 2013 CONCLUSIONS: In this study, we demonstrated that the effect of celastrol on apoptosis is due to miR-146a inhibition of NF-kappaB activity. celastrol 63-72 microRNA 146a Homo sapiens 96-104 23528241-6 2013 In contrast, in EBV positive cell lines of activated B cell phenotype, and EBV negative BL cell lines the invariably unmethylated 5" regulatory sequences of active miR-146a promoters were enriched in the euchromatic histone modification marks acetylated histone H3, acetylated histone H4, and histone H3 dimethylated at lysine 4. Lysine 320-326 microRNA 146a Homo sapiens 164-172 23459235-5 2013 We identified seven microRNAs (miR-124a, miR-146a &amp; b, miR-185, miR-16 and let-7a &amp; b), which displayed significant differential expression in normal prostate tissue from men with prostate cancer compared to both cancer negative control groups. Adenosine Monophosphate 55-58 microRNA 146a Homo sapiens 41-49 23459235-5 2013 We identified seven microRNAs (miR-124a, miR-146a &amp; b, miR-185, miR-16 and let-7a &amp; b), which displayed significant differential expression in normal prostate tissue from men with prostate cancer compared to both cancer negative control groups. Adenosine Monophosphate 55-58 microRNA 146a Homo sapiens 41-49 23459235-5 2013 We identified seven microRNAs (miR-124a, miR-146a &amp; b, miR-185, miR-16 and let-7a &amp; b), which displayed significant differential expression in normal prostate tissue from men with prostate cancer compared to both cancer negative control groups. Adenosine Monophosphate 55-58 microRNA 146a Homo sapiens 41-49 23555954-6 2013 On the other hand, miR-146a enhanced the inhibition of cell proliferation by drugs targeting EGFR, including both TKIs (gefitinib, erlotinib, and afatinib) and a monoclonal antibody (cetuximab). Gefitinib 120-129 microRNA 146a Homo sapiens 19-27 23621234-10 2013 In conclusion, expression changes in miRNAs of miR-146a, miR-100, miR-425, miR-193a-3p and, miR-106b in metformin-treated cells may be important. Metformin 104-113 microRNA 146a Homo sapiens 47-55 23555954-6 2013 On the other hand, miR-146a enhanced the inhibition of cell proliferation by drugs targeting EGFR, including both TKIs (gefitinib, erlotinib, and afatinib) and a monoclonal antibody (cetuximab). Erlotinib Hydrochloride 131-140 microRNA 146a Homo sapiens 19-27 23555954-6 2013 On the other hand, miR-146a enhanced the inhibition of cell proliferation by drugs targeting EGFR, including both TKIs (gefitinib, erlotinib, and afatinib) and a monoclonal antibody (cetuximab). Afatinib 146-154 microRNA 146a Homo sapiens 19-27 23555954-9 2013 We also found, in clinical formalin fixed paraffin embedded (FFPE) lung cancer samples, that low expression of miR-146a was correlated with advanced clinical TNM stages and distant metastasis in NSCLC (P<0.05). Formaldehyde 27-35 microRNA 146a Homo sapiens 111-119 23555954-9 2013 We also found, in clinical formalin fixed paraffin embedded (FFPE) lung cancer samples, that low expression of miR-146a was correlated with advanced clinical TNM stages and distant metastasis in NSCLC (P<0.05). Paraffin 42-50 microRNA 146a Homo sapiens 111-119 23554878-7 2013 Both miR-146a and miR-150 increase the number of residual surviving cells by 2-4 fold when challenged with lethal cisplatin concentrations. Cisplatin 114-123 microRNA 146a Homo sapiens 5-13 21347720-4 2012 The cell growth rate of MKN-45 gastric cancer cells transfected with miR-146a mimics was examined by MTT assay. monooxyethylene trimethylolpropane tristearate 101-104 microRNA 146a Homo sapiens 69-77 23756365-0 2013 Morphine induced exacerbation of sepsis is mediated by tempering endotoxin tolerance through modulation of miR-146a. Morphine 0-8 microRNA 146a Homo sapiens 107-115 23756365-3 2013 Morphine was found to down-regulate endotoxin/LPS induced miR-146a and 155 in macrophages. Morphine 0-8 microRNA 146a Homo sapiens 58-66 23756365-4 2013 However, only miR-146a over expression, but not miR-155 abrogates morphine mediated hyper-inflammation. Morphine 66-74 microRNA 146a Homo sapiens 14-22 23756365-5 2013 Conversely, antagonizing miR-146a (but not miR-155) heightened the severity of morphine-mediated hyper-inflammation. Morphine 79-87 microRNA 146a Homo sapiens 25-33 23756365-6 2013 These results suggest that miR-146a acts as a molecular switch controlling hyper-inflammation in clinical and/or recreational use of morphine. Morphine 133-141 microRNA 146a Homo sapiens 27-35 23146644-15 2012 CONCLUSIONS: The results suggested that LPS is able to increase the migration of DPCs by modulating the miR-146a-TRAF6/IRAK1 regulatory cascade. dpcs 81-85 microRNA 146a Homo sapiens 104-112 22711166-4 2012 A wound-healing assay and a Transwell assay were used to investigate the impact of miR-146a on the migratory and invasive abilities of MKN-45 cells in vitro. mkn-45 159-165 microRNA 146a Homo sapiens 95-103 21347720-9 2012 The MTT assay showed that introduction of miR-146a inhibited cell proliferation in MKN-45 cells (P < 0.05). monooxyethylene trimethylolpropane tristearate 4-7 microRNA 146a Homo sapiens 42-50 22311030-5 2012 Two common polymorphisms in pre-miRNAs: Homo sapiens miRNA-146a (hsa-mir-146a) (rs291016, guanine to cytosine [G-C]) and hsa-mir-499 (rs3746444; adenine to guanine [C-T]) were genotyped by PCR-Restriction Fragment Length Polymorphism and confirmed by bidirectional DNA sequencing. Guanine 90-97 microRNA 146a Homo sapiens 53-63 22969965-0 2012 Clinical and prognostic significance of miR-155 and miR-146a expression levels in formalin-fixed/paraffin-embedded tissue of patients with diffuse large B-cell lymphoma. Formaldehyde 82-90 microRNA 146a Homo sapiens 52-60 22949852-6 2012 BPA exposure of human placental cell lines has been shown to alter microRNA expression levels, and specifically, miR-146a was strongly induced by BPA treatment. bisphenol A 0-3 microRNA 146a Homo sapiens 113-121 22949852-6 2012 BPA exposure of human placental cell lines has been shown to alter microRNA expression levels, and specifically, miR-146a was strongly induced by BPA treatment. bisphenol A 146-149 microRNA 146a Homo sapiens 113-121 22043907-3 2011 Upregulated miRNA-146a is also observed in pro-inflammatory cytokine-, Abeta42 peptide- and neurotoxic metal-induced, oxidatively stressed human neuronal-glial primary cell cocultures, in murine scrapie and in Alzheimer"s disease (AD) brain. Metals 103-108 microRNA 146a Homo sapiens 12-22 22099153-0 2011 Up-regulation of NF-kB-sensitive miRNA-125b and miRNA-146a in metal sulfate-stressed human astroglial (HAG) primary cell cultures. metal sulfate 62-75 microRNA 146a Homo sapiens 48-58 22099153-3 2011 In this study we analyzed abundances miRNA-125b and miRNA-146a in magnesium-, iron-, gallium, and aluminum-sulfate-stressed human-astroglial (HAG) cells, a structural and immune-responsive brain cell type. Magnesium 66-75 microRNA 146a Homo sapiens 52-62 22099153-3 2011 In this study we analyzed abundances miRNA-125b and miRNA-146a in magnesium-, iron-, gallium, and aluminum-sulfate-stressed human-astroglial (HAG) cells, a structural and immune-responsive brain cell type. Iron 78-82 microRNA 146a Homo sapiens 52-62 22099153-3 2011 In this study we analyzed abundances miRNA-125b and miRNA-146a in magnesium-, iron-, gallium, and aluminum-sulfate-stressed human-astroglial (HAG) cells, a structural and immune-responsive brain cell type. Gallium 85-92 microRNA 146a Homo sapiens 52-62 22099153-3 2011 In this study we analyzed abundances miRNA-125b and miRNA-146a in magnesium-, iron-, gallium, and aluminum-sulfate-stressed human-astroglial (HAG) cells, a structural and immune-responsive brain cell type. aluminum sulfate 98-114 microRNA 146a Homo sapiens 52-62 22099153-4 2011 The combination of iron- plus aluminum-sulfate was found to be significantly synergistic in up-regulating reactive oxygen species (ROS) abundance, NF-kB-DNA binding and miRNA-125b and miRNA-146a expression. Iron 19-23 microRNA 146a Homo sapiens 184-194 22099153-4 2011 The combination of iron- plus aluminum-sulfate was found to be significantly synergistic in up-regulating reactive oxygen species (ROS) abundance, NF-kB-DNA binding and miRNA-125b and miRNA-146a expression. aluminum sulfate 30-46 microRNA 146a Homo sapiens 184-194 21329689-4 2011 MiR-146a significantly reduces intracellular LDL cholesterol content and secretion of interleukin 6, interleukin 8, chemokine (C-C motif) ligand 2 and matrix metallopeptidase 9. Cholesterol 49-60 microRNA 146a Homo sapiens 0-8 20934487-3 2011 Inducible expression of miRNA-146a was found to be significantly up-regulated in a primary co-culture of human neuronal-glial (HNG) cells stressed using interleukin1-beta (IL-1beta), and this up-regulation was quenched using specific NF-kB inhibitors including curcumin. Curcumin 261-269 microRNA 146a Homo sapiens 24-34 20937840-7 2010 The NF-kappaB inhibitors curcumin, pyrrolidine dithiocarbamate or CAY10512 abrogated both IRAK-2 and miRNA-146a expression, whereas IRAK-1 was up-regulated. Curcumin 25-33 microRNA 146a Homo sapiens 101-111 21949733-3 2011 Although expression of these selected miRNAs did not differ between treatment-naive (n = 36) and interferon-beta treated RRMS patients (n = 18), expression of miR-146a and miR-142-3p was significantly lower in glatiramer acetate (GA) treated RRMS patients (n = 20) suggesting that GA, at least in part, restores the expression of deregulated miRNAs in MS. Glatiramer Acetate 210-228 microRNA 146a Homo sapiens 159-167 20937840-7 2010 The NF-kappaB inhibitors curcumin, pyrrolidine dithiocarbamate or CAY10512 abrogated both IRAK-2 and miRNA-146a expression, whereas IRAK-1 was up-regulated. pyrrolidine dithiocarbamic acid 35-62 microRNA 146a Homo sapiens 101-111 20937840-7 2010 The NF-kappaB inhibitors curcumin, pyrrolidine dithiocarbamate or CAY10512 abrogated both IRAK-2 and miRNA-146a expression, whereas IRAK-1 was up-regulated. NF-kB Activation Inhibitor IV 66-74 microRNA 146a Homo sapiens 101-111 20522791-0 2010 Reduced miR-146a increases prostaglandin E2in chronic obstructive pulmonary disease fibroblasts. Dinoprostone 27-43 microRNA 146a Homo sapiens 8-16 20952466-8 2010 After treatment with calcitriol for 6 months, serum miR-146a level of SLE patients increased significantly (p < 0.001), and its change inversely correlated with the level of calcium-phosphate product (r = -0.466, p = 0.003). Calcitriol 21-31 microRNA 146a Homo sapiens 52-60 20952466-8 2010 After treatment with calcitriol for 6 months, serum miR-146a level of SLE patients increased significantly (p < 0.001), and its change inversely correlated with the level of calcium-phosphate product (r = -0.466, p = 0.003). calcium phosphate 177-194 microRNA 146a Homo sapiens 52-60 20656888-0 2010 Diazoxide potentiates mesenchymal stem cell survival via NF-kappaB-dependent miR-146a expression by targeting Fas. Diazoxide 0-9 microRNA 146a Homo sapiens 77-85 20647767-4 2010 TCL-1 cells exposed to both nicotine and benzo(a)pyrene exhibited significant, dose-dependent downregulation of miR-146a. Nicotine 28-36 microRNA 146a Homo sapiens 112-120 20647767-4 2010 TCL-1 cells exposed to both nicotine and benzo(a)pyrene exhibited significant, dose-dependent downregulation of miR-146a. Benzo(a)pyrene 41-55 microRNA 146a Homo sapiens 112-120 20195282-6 2010 Furthermore, we showed that miR-146a treatment could modulate the Th1 differentiation through posttranscriptional enhancing the T-bet pathway in PBMCs. t-bet 128-133 microRNA 146a Homo sapiens 28-36 20495188-8 2010 After Dox treatment, overexpression of miR-146a, as well as that of siRNA against ErbB4, induced cell death in cardiomyocytes. Doxorubicin 6-9 microRNA 146a Homo sapiens 39-47 20495188-11 2010 When miR-146a "decoy" genes were introduced into cardiomyocytes, ErbB4 expression was up-regulated and Dox-induced cell death was reduced. Doxorubicin 103-106 microRNA 146a Homo sapiens 5-13 20495188-12 2010 CONCLUSION: These findings suggested that the up-regulation of miR-146a after Dox treatment is involved in acute Dox-induced cardiotoxicity by targeting ErbB4. Doxorubicin 78-81 microRNA 146a Homo sapiens 63-71 20495188-12 2010 CONCLUSION: These findings suggested that the up-regulation of miR-146a after Dox treatment is involved in acute Dox-induced cardiotoxicity by targeting ErbB4. Doxorubicin 113-116 microRNA 146a Homo sapiens 63-71 20577838-5 2010 These data suggested that miR-146a might influence proliferation of APL cells through TGF-beta1/Smad signal transduction pathway during ATRA induction. Tretinoin 136-140 microRNA 146a Homo sapiens 26-34 20417706-6 2010 Real-time PCR results confirmed that miR-146a was particularly strongly induced and its overexpression in cells led to slower proliferation as well as higher sensitivity to the DNA damaging agent, bleomycin. Bleomycin 197-206 microRNA 146a Homo sapiens 37-45 20061215-3 2010 OBJECTIVES: We evaluated the effects of exposure to PM and PM metal components on candidate miRNAs (miR-222, miR-21, and miR-146a) related with oxidative stress and inflammatory processes in 63 workers at an electric-furnace steel plant. Metals 62-67 microRNA 146a Homo sapiens 121-129 20061215-9 2010 Postexposure expression of miR-146a was not significantly different from baseline (baseline = 0.61 +/- 2.42, postexposure = 1.90 +/- 3.94, p = 0.19) but was negatively correlated with exposure to lead (beta = -0.51, p = 0.011) and cadmium (beta = -0.42, p = 0.04). Cadmium 231-238 microRNA 146a Homo sapiens 27-35 20110513-6 2010 The genesis of alkaline phosphatase and the up-regulation of miR-146a were induced by ascorbic acid in the I-PDL cells and primary PDL cells. Ascorbic Acid 86-99 microRNA 146a Homo sapiens 61-69 20124483-6 2010 Treatment of pancreatic cancer cells with the natural products 3,3"-diinodolylmethane (DIM) or isoflavone, which increased miR-146a expression, caused a downregulation of EGFR, MTA-2, IRAK-1, and NF-kappaB, resulting in an inhibition of pancreatic cancer cell invasion. 3,3"-diinodolylmethane 63-85 microRNA 146a Homo sapiens 123-131 20124483-6 2010 Treatment of pancreatic cancer cells with the natural products 3,3"-diinodolylmethane (DIM) or isoflavone, which increased miR-146a expression, caused a downregulation of EGFR, MTA-2, IRAK-1, and NF-kappaB, resulting in an inhibition of pancreatic cancer cell invasion. 1,4-dideoxy-1,4-iminomannitol 87-90 microRNA 146a Homo sapiens 123-131 20124483-6 2010 Treatment of pancreatic cancer cells with the natural products 3,3"-diinodolylmethane (DIM) or isoflavone, which increased miR-146a expression, caused a downregulation of EGFR, MTA-2, IRAK-1, and NF-kappaB, resulting in an inhibition of pancreatic cancer cell invasion. Isoflavones 95-105 microRNA 146a Homo sapiens 123-131 19918258-5 2010 The results showed transfected miR-146a could produce a comparable increase in the number of GWB and this was accompanied by a reduction in major cytokines/chemokines induced by LPS. 4-[(CYCLOPROPYLETHYNYL)OXY]-6-FLUORO-3-ISOPROPYLQUINOLIN-2(1H)-ONE 93-96 microRNA 146a Homo sapiens 31-39 19390647-3 2009 Bacterial lipopolysaccharide (LPS) induces a reactive oxygen species-/NF-kappaB-dependent pathway which increases the expression of the anti-inflammatory miR-146a. Reactive Oxygen Species 45-68 microRNA 146a Homo sapiens 154-162 19540598-0 2009 Characterization of an NF-kappaB-regulated, miRNA-146a-mediated down-regulation of complement factor H (CFH) in metal-sulfate-stressed human brain cells. metal-sulfate 112-125 microRNA 146a Homo sapiens 44-54 19540598-3 2009 Here we provide evidence in human neural (HN) cells of an aluminum-sulfate- and reactive oxygen species (ROS)-mediated up-regulation of an NF-kappaB-sensitive miRNA-146a that down-regulates the expression of complement factor H (CFH), an important repressor of inflammation. aluminum sulfate 58-74 microRNA 146a Homo sapiens 159-169 19540598-3 2009 Here we provide evidence in human neural (HN) cells of an aluminum-sulfate- and reactive oxygen species (ROS)-mediated up-regulation of an NF-kappaB-sensitive miRNA-146a that down-regulates the expression of complement factor H (CFH), an important repressor of inflammation. Reactive Oxygen Species 80-103 microRNA 146a Homo sapiens 159-169 19540598-3 2009 Here we provide evidence in human neural (HN) cells of an aluminum-sulfate- and reactive oxygen species (ROS)-mediated up-regulation of an NF-kappaB-sensitive miRNA-146a that down-regulates the expression of complement factor H (CFH), an important repressor of inflammation. Reactive Oxygen Species 105-108 microRNA 146a Homo sapiens 159-169 19540598-6 2009 An NF-kappaB-containing miRNA-146a-promoter-luciferase reporter construct transfected into HN cells showed significant up-regulation of miRNA-146a after aluminum-sulfate treatment that corresponded to decreased CFH gene expression. aluminum sulfate 153-169 microRNA 146a Homo sapiens 24-34 19540598-6 2009 An NF-kappaB-containing miRNA-146a-promoter-luciferase reporter construct transfected into HN cells showed significant up-regulation of miRNA-146a after aluminum-sulfate treatment that corresponded to decreased CFH gene expression. aluminum sulfate 153-169 microRNA 146a Homo sapiens 136-146 19540598-7 2009 These data suggest that (1) as in AD brain, NF-kappaB-sensitive, miRNA-146a-mediated, modulation of CFH gene expression may contribute to inflammatory responses in aluminum-stressed HN cells, and (2) underscores the potential of nanomolar aluminum to drive genotoxic mechanisms characteristic of neurodegenerative disease processes. Aluminum 164-172 microRNA 146a Homo sapiens 65-75 19540598-7 2009 These data suggest that (1) as in AD brain, NF-kappaB-sensitive, miRNA-146a-mediated, modulation of CFH gene expression may contribute to inflammatory responses in aluminum-stressed HN cells, and (2) underscores the potential of nanomolar aluminum to drive genotoxic mechanisms characteristic of neurodegenerative disease processes. Aluminum 239-247 microRNA 146a Homo sapiens 65-75 19390647-5 2009 Preincubation of human monocytic THP-1 cells with ubiquinol-10 reduced the LPS-induced expression level of miR-146a to 78.9 +/- 13.22%. ubiquinol-10 50-62 microRNA 146a Homo sapiens 107-115 19390647-7 2009 From these consistent in vitro and in vivo data, we conclude that ubiquinol-10 may fine-tune the inflammatory response via moderate reduction of miR-146a expression. ubiquinol-10 66-78 microRNA 146a Homo sapiens 145-153 18801740-6 2008 Incubation of an antisense oligonucleotide to miRNA-146a (anti-miRNA-146a; AM-146a) was found to restore CFH expression levels. Oligonucleotides 27-42 microRNA 146a Homo sapiens 46-56 18801740-6 2008 Incubation of an antisense oligonucleotide to miRNA-146a (anti-miRNA-146a; AM-146a) was found to restore CFH expression levels. Oligonucleotides 27-42 microRNA 146a Homo sapiens 63-73 18174313-7 2008 Given that ROCK1 is one of the key kinases for the activation of hyaluronan (HA)-mediated HRPC transformation in vivo and in PC3 cells, mir-146a may function as a tumor-suppressor gene in modulating HA/ROCK1-mediated tumorigenecity in androgen-dependent prostate cancer. Hyaluronic Acid 65-75 microRNA 146a Homo sapiens 136-144 18383392-7 2008 Constitutive expression of both miR-155 and miR-146a was higher in RASFs than in those from patients with osteoarthritis (OA), and expression of miR-155 could be further induced by TNFalpha, interleukin-1beta, lipopolysaccharide, poly(I-C), and bacterial lipoprotein. Poly I-C 230-238 microRNA 146a Homo sapiens 44-52