Downregulation of miR-181a alleviates renal fibrosis in diabetic nephropathy mice.

Accumulating evidence suggests that microRNAs are important regulators in the pathology of diabetes and its relevant renal injures. Little is known about the role of miR-181a in development of diabetic nephropathy. The aim of our present study was to investigate levels of miR-181a in diabetic nephropathy and explore its underlying mechanism. In the present study, Db/db and db/m mice were randomized into groups with 12 mice in each: db/m group, db/db group, and antagomiR-181a-treated db/db group. Changes in renal cortical sections were studied by histopathology. Mouse mesangial cells transfected with miR-mimic or miR-inhibitor and cell growth was measured using MTT assay. Levels of miR-181a expression were detected using qRT-PCR under different conditions. Indexes were measured using qRT-PCR and Western blot. Our results show that downregulation of miR-181a could alleviate pathological changes of diabetic nephropathy in mice. miR-181a expression was significantly upregulated in mouse mesaginal cells (P<0.05). Overexpression of miR-181a promoted extracellular matrix under high glucose by measuring related indexes such as collagen I, collagen IV, and fibronectin, which could be reversed by miR-181a inhibitors (P<0.05). Upregulation of miR-181a suppressed expression of TβRIII by binding with 3'-UTR. These findings suggest miR-181a plays as an important role in renal fibrosis of diabetic nephropathy in an animal model.