MiR‐130b increases fibrosis of HMC cells by regulating the TGF‐β1 pathway in diabetic nephropathy

Abstract Basement membrane thickening, glomerular hypertrophy, and deposition of multiple extracellular matrix characterize the pathological basis of diabetic nephropathy (DN), a condition which ultimately leads to glomerular and renal interstitial fibrosis. Here, we identified a novel microRNA, miR‐130b, and investigated its role and therapeutic efficacy in alleviating DN. Introduction of miR‐130b dramatically increased cell growth and fibrosis in DN cells. We found that transforming growth factor (TGF)‐β1 was a functional target of miR‐130b in human glomerular mesangial cells (HMCs) and overexpression of miR‐130b increased expressions of the downstream signaling molecules of TGF‐β1, t‐Smad2/3, p‐Smad2/3, and SMAD4. An ectopic application of miR‐130b increased messenger RNA and protein expressions of collagen type I (colI), colIV, and fibronectin, whose expression levels were correlated with the expression of miR‐130b. Taken together, the findings of this study reveal that miR‐130b in HMC cells plays an important role in fibrosis regulation and may thus be involved with the pathogenesis of DN. Therefore, miR‐130b may serve as a novel therapeutic target for the prevention and the treatment of DN.