MicroRNA-30c suppresses the pro-fibrogenic effects of cardiac fibroblasts induced by TGF-?1 and prevents atrial fibrosis by targeting TGF?RII.

ABSTRACT: Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). Recent data have suggested that microRNA-30c (miR-30c) is involved in fibrotic remodelling and cancer development, but the specific role of miR-30c in atrial fibrosis remains unclear. The purpose of this study was to investigate the role of miR-30c in atrial fibrosis and its underlying mechanisms through in vivo and in vitro experiments. Our results indicate that miR-30c is significantly down-regulated in the rat abdominal aortic constriction (AAC) model and in the cellular model of fibrosis induced by transforming growth factor-?1 (TGF-?1). Overexpression of miR-30c in cardiac fibroblasts (CFs) markedly inhibits CF proliferation, differentiation, migration and collagen production, whereas decrease in miR-30c leads to the opposite results. Moreover, we identified TGF?RII as a target of miR-30c. Finally, transferring adeno-associated virus 9 (AAV9)-miR-30c into the inferior vena cava of rats attenuated fibrosis in the left atrium following AAC. These data indicate that miR-30c attenuates atrial fibrosis via inhibition of CF proliferation, differentiation, migration and collagen production by targeting TGF?RII, suggesting that miR-30c might be a novel potential therapeutic target for preventing atrial fibrosis.

SUBMITTER: Xu J 

PROVIDER: S-EPMC5980214 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature