MicroRNA-488 regulates diabetic nephropathy via TGF-β1 pathway

OBJECTIVE: The aim of this study was to clarify the biological roles of microRNA-488 and transforming growth factor beta 1 (TGF-beta 1) pathway in the occurrence and progression of diabetic nephropathy (DN). MATERIALS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expressions of microRNA-488, fibrinogen factors coll, coIIV, and fibronectin (FN) in Human mesangial cells (HMCs) with high-glucose or low-glucose treatment. After transfection of microRNA-488 mimics or inhibitor. expression levels of coll, coIIV, and FN in HMCs were determined by qRT-PCR and Western blot. Their expressions in HMC cells treated with different doses of TGF-beta 1 at different time points were also detected. Finally, we evaluated the potential influence of microRNA-488 on TGF-beta 1-induced fibrosis of HMC cells by qRT-PCR. RESULTS: Compared with low-glucose treatment, the expression of microRNA-488 markedly increased in HMCs treated with high-glucose, as well as coll, coIIV, and FN. Overexpression of microRNA-488 remarkably upregulated mRNA and protein levels of coll, coIIV, and FN. whereas microRNA-488 knockdown downregulated their levels. Expression levels of microRNA-488, coll, coIIV, and FN gradually upregulated with the increase of TGF-beta 1 dose and treatment duration. CONCLUSIONS: MicroRNA-488 regulates the development of diabetic nephropathy-induced fibrosis by TGF-beta 1 pathway.