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

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 decreased col-IV, FN, GSI, GBM, GA, MRA/CLA and ACR (p < 0.05) and, in contrast, slightly but significantly increased Ccr (p < 0.05). In conclusion, our results suggested that loss of miR-30c may contribute to the pathogenesis of DN by inhibiting target CTGF expression; replenishing miR-30c may ameliorate renal structure and function by reducing renal fibrosis in DN.