Article ID Journal Published Year Pages File Type
5902072 Journal of Diabetes and its Complications 2016 27 Pages PDF
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 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.
Related Topics
Life Sciences Biochemistry, Genetics and Molecular Biology Endocrinology
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