Downregulation of miR-30c promotes renal fibrosis by target CTGF in diabetic nephropathy

Journal of Diabetes and Its Complications
Jin-yang WangJ Yang

Abstract

MicroRNAs (miRs) play important roles in initiation and progression of many pathologic processes. However, the role of miR-30c in diabetic nephropathy (DN) remains unclear. This study was to determine whether miR-30c was involved in the mechanism of renal fibrosis by inhibiting target CTGF expression in DN. In this study, In Situ Hybridization(ISH), RT-PCR, cell transfection, western blotting and laser confocal telescope were used, respectively. ISH showed that miR-30c, concentrated in cytoplasmic foci in the proximity of the nucleus, was mainly localized in glomerular and renal tubular epithelial cells within the cortex. RT-PCR showed that miR-30c expression was significantly decreased in DN (p<0.05), consistent with of the results of ISH. Luciferase reporter gene assays showed that CTGF was a validated target of miR-30c. Furthermore, miR-30c overexpression directly decreased CTGF mRNA and protein. Conversely, miR-30c inhibitor enhanced CTGF expression. Interestingly, miR-30c expression was negatively correlated with ACR (r=-0.870, P=0.003) and positively correlated with Ccr (r=0.8230, P=0.01), whereas it was uncorrelated with KW/BW, SBP, HbA1C, HOMR-IR and T-Cho (p>0.05). More importantly, miR-30c mimics significantly decreas...Continue Reading

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