ArticleActa pharmacologica Sinica2013
Over-production of nitric oxide by oxidative stress-induced activation of the TGF-β1/PI3K/Akt pathway in mesangial cells cultured in high glucose.
Article in Acta pharmacologica Sinica, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosisWorld journal of diabetes · 2025Article
- Mubritinib enhanced the inhibiting function of cisplatin in lung cancer by interfering with mitochondrial function.Thoracic cancer · 2022Article
- Cilostazol ameliorates diabetic nephropathy by inhibiting highglucose- induced apoptosis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020Article
- MiR-29b expression is altered in crescent formation of HSPN and accelerates Ang II-induced mesangial cell activation.World journal of pediatrics : WJP · 2020Article
- VASH-1 Regulates Oxidative Stress and Fibrosis in Diabetic Kidney Disease via SIRT1/HIF1α and TGFβ1/Smad3 Signaling Pathways.Frontiers in molecular biosciences · 2020Article
- TRPM7 channels play a role in high glucose-induced endoplasmic reticulum stress and neuronal cell apoptosis.The Journal of biological chemistry · 2018Article
- ReducedBioMed research international · 2018Article
- CAPE-Oncotarget · 2017Article
- Human Peritoneal Mesothelial Cell Death Induced by High-Glucose Hypertonic Solution Involves CaFrontiers in physiology · 2017Article
- Protective role of propofol on the kidney during early unilateral ureteral obstruction through inhibition of epithelial-mesenchymal transition.American journal of translational research · 2016Article
- Overexpression of the FoxO1 Ameliorates Mesangial Cell Dysfunction in Male Diabetic Rats.Molecular endocrinology (Baltimore, Md.) · 2015Article
- NADPH oxidase-dependent production of reactive oxygen species induces endoplasmatic reticulum stress in neutrophil-like HL60 cells.PloS one · 2015Article
- Selective α1B- and α1D-adrenoceptor antagonists suppress noradrenaline-induced activation, proliferation and ECM secretion of rat hepatic stellate cells in vitro.Acta pharmacologica Sinica · 2014Article
- Therapeutic effects of DZ2002, a reversible SAHH inhibitor, on lupus-prone NZB×NZW F1 mice via interference with TLR-mediated APC response.Acta pharmacologica Sinica · 2014Article
- P2X7 receptor-nitric oxide interaction mediates apoptosis in mouse immortalized mesangial cells exposed to high glucose.Jornal brasileiro de nefrologiaArticle
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8 authors.
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Abstract
aimTo investigate whether NO over-production in rat mesangial cells cultured in high glucose (HG) is related to activation of the TGF-β1/PI3K/Akt pathway.
methodsRat mesangial cells line (HBZY-1) was exposed to HG (24.44 mmol/L) or H2O2 (10 μmol/L) for 16 h. NO release was quantified using the Griess assay. The TGF-β1 level was measured using ELISA. The protein expression of p-Akt, t-Akt, Bim, and iNOS was examined by Western blotting. The mRNA levels of TGF-β1 and Bim were measured using RT-PCR. The cell proliferation rate was estimated using a BrdU incorporation assay.
resultsTreatment of the cells with HG, H2O2, or TGF-β1 (5 ng/mL) significantly increased the NO level that was substantially inhibited by co-treatment with the NADPH oxidase inhibitor diphenylene iodonium (DPI), TGF-β1 inhibitor SB431542, or PI3K inhibitor LY294002. Both HG and H2O2 significantly increased the protein and mRNA levels of TGF-β1 in the cells, and HG-induced increases of TGF-β1 protein and mRNA were blocked by co-treatment with DPI. Furthermore, the treatment with HG or H2O2 significantly increased the expression of phosphorylated Akt and iNOS and cell proliferation rate, which was blocked by co-treatment with DPI, SB431542, or LY294002. Moreover, the treatment with HG or H2O2 significantly inhibited Bim protein and mRNA expression, which was reversed by co-treatment with DPI, SB431542, or LY294002.
conclusionThe results demonstrate that high glucose causes oxidative stress and NO over-production in rat mesangial cells in vitro via decreasing Bim and increasing iNOS, which are at least partially mediated by the TGF-β1/PI3K/Akt pathway.
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