MicroRNA-488 regulates diabetic nephropathy via TGF-β1 pathway.

Abstract

The aim of this study was to clarify the biological roles of microRNA-488 and transforming growth factor β1 (TGF-β1) pathway in the occurrence and progression of diabetic nephropathy (DN). Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect the expressions of microRNA-488, fibrinogen factors coII, 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 coII, coIIV, and FN in HMCs were determined by qRT-PCR and Western blot. Their expressions in HMC cells treated with different doses of TGF-β1 at different time points were also detected. Finally, we evaluated the potential influence of microRNA-488 on TGF-β1-induced fibrosis of HMC cells by qRT-PCR. Compared with low-glucose treatment, the expression of microRNA-488 markedly increased in HMCs treated with high-glucose, as well as coII, coIIV, and FN. Overexpression of microRNA-488 remarkably upregulated mRNA and protein levels of coII, coIIV, and FN, whereas microRNA-488 knockdown downregulated their levels. Expression levels of microRNA-488, coII, coIIV, and FN gradually upregulated with the increase of TGF-β1 dose and treatment duration. MicroRNA-488 regulates the development of diabetic nephropathy-induced fibrosis by TGF-β1 pathway.