Study on the molecular mechanism of miR-25 expression in the regulation of diabetic nephropathy

Objective To investigate the molecular mechanism of microRNA-25 (miR-25) expression in the regulation of diabetic nephropathy (DN) formation. Methods Diabetic nephropathy model (Dia group) mice and model HK-2 cells were induced by streptozotocin and high glucose induction method, respectively. Fluorescence quantitative PCR was used to detect the quality of kidney in normal mice (Con group) and Dia group mice. LVWI and the expression levels of miR-25, DAB2IP, P38-MAPK, and P-AKT mRNA in kidneys, and the expression levels of miR-25, DAB2IP, P38-MAPK, and P-AKT mRNA in HK-2 cells were detected. MiR-25 mimics were used to overexpress miR-25 in HK-2 cells, and Western blot was used to detect the expression of DAB2IP, P38-MAPK, and P-AKT protein. Results All mice in the Dia group were successfully modeled. The renal mass index, relative expression of P38-MAPK, P-AKT, and DAB2IP mRNA of Dia group were significantly higher than those of Con group, the relative expression of miR-25 in the kidney was significantly lower than that of Con group (P<0.05). The relative expression level of miR-25 in HK-2 cells of model group was significantly lower than that of normal HK-2 cells (P<0.05), the relative expression levels of P38-MAPK, P-AKT, and DAB2IP mRNA in HK-2 cells of model group were significantly higher than those of normal HK-2 cells (P<0.05). After HK-2 cells and model HK-2 cells were transfected with miR-25 mimics, Western blot results showed that the expression of P-AKT and P38-MAPK in model HK-2 cells significantly down-regulated (P<0.05). Conclusion High expression of miR-25 can inhibit the expression of P-AKT and P38-MAPK, and may promote the occurrence of DN through the JNK signaling pathway. Key words: Diabetic nephropathy; miRNA-25; P-AKT; P38-MAPK