کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8451951 | 1547699 | 2017 | 28 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The crosstalk between Sirt1 and Keap1/Nrf2/ARE anti-oxidative pathway forms a positive feedback loop to inhibit FN and TGF-β1 expressions in rat glomerular mesangial cells
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کلمات کلیدی
DCFH-DAKeap1/Nrf2/ARE pathwayAdvanced glycation-end products2′, 7′-dichlorofluorescin diacetateGMCstert-butylhydroquinoneAGEsECMHO-1Nrf2Sirt1TBHQTGF-β1BSA - BSAkeap1 - buy1NAD+ - NAD +ROS - ROSElectrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزbovine serum albumin - آلبومین سرم گاوsodium dodecyl sulfate-polyacrylamide gel electrophoresis - الکتروفورز ژل دوده سولفات سدیم پلی آکریل آمیدOSS - ایالات متحدهTransforming growth factor-β1 - تبدیل فاکتور رشد β1Immunoprecipitation - تخریب ایمنیOxidative stress - تنش اکسیداتیوSOD - سدglomerular mesangial cells - سلول های مزانژی گلومرولیEMSA یا electrophoretic mobility shift assay - سنجش تغییر تحرک الکتروفورتیکSuperoxide dismutase - سوکسوکس دیسموتازanti-oxidant response element - عنصر پاسخ anti-oxidantnuclear factor erythroid 2-related factor 2 - فاکتور هسته ای عامل erythroid 2 مرتبط 2Fibronectin - فیبرونکتینExtracellular matrix - ماتریکس خارج سلولیDiabetic nephropathy - نفروپاتی دیابتیARE - هستندheme oxygenase 1 - همای اکسیژناز 1Reactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Oxidative stress aroused by advanced glycation-end products (AGEs) is a culprit in the pathological progression of diabetic nephropathy. Both Sirt1 and the Keap1/Nrf2/ARE anti-oxidative pathway exert crucial inhibitory effects on the development of diabetic nephropathy. Our previous study has confirmed that Sirt1 activation can inhibit the upregulation of fibronectin (FN) and transforming growth factor-β1 (TGF-β1) by promoting Keap1/Nrf2/ARE pathway in glomerular mesangial cells (GMCs) challenged with AGEs. However, the underlying mechanism needs further investigation. Here, we found that concomitant with deacetylating and reducing the ubiquitination levels of Nrf2, Sirt1 significantly enhanced the activity of Keap1/Nrf2/ARE pathway including decreasing Keap1 expression, promoting the nuclear content, ARE-binding ability, and transcriptional activity of Nrf2, augmenting the protein levels of heme oxygenase 1, a target gene of Nrf2, which eventually quenched ROS overproduction and alleviating FN and TGF-β1 accumulation in AGEs-treated GMCs. And depletion of Nrf2 blocked those renoprotective effects of Sirt1. Interestingly, Nrf2 also positively regulated Sirt1 at the protein expression and deacetylase activity levels as evidenced by tert-Butylhydroquinone and specific siRNA targeting Nrf2 to downregulate FN and TGF-β1. In conclusion, the current study basically demonstrated that the crosstalk between Sirt1 and Keap1/Nrf2/ARE anti-oxidative pathway forms a positive feedback loop to inhibit the protein expressions of FN and TGF-β1 in AGEs-treated GMCs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Experimental Cell Research - Volume 361, Issue 1, 1 December 2017, Pages 63-72
Journal: Experimental Cell Research - Volume 361, Issue 1, 1 December 2017, Pages 63-72
نویسندگان
Kaipeng Huang, Xiang Gao, Wentao Wei,