<i>miR-139-5p</i> inhibits isoproterenol-induced cardiac hypertrophy by targetting c-Jun

Abstract

Hypertrophic cardiomyopathy (HCM) is a serious monogenic disease characterized by cardiac hypertrophy, fibrosis, sudden cardiac death, and heart failure. Previously, we identified that <i>miR-139-5p</i> was down-regulated in HCM patients. However, the regulatory effects of <i>miR-139-5p</i> remain unclear. Thus, we investigated the role of <i>miR-139-5p</i> in the regulation of cardiac hypertrophy. The expression of <i>miR-139-5p</i> in left ventricular tissues in HCM patients and mice subjected to transverse aortic constriction (TAC) was significantly down-regulated. Knockdown of <i>miR-139-5p</i> expression in neonatal rat cardiomyocytes (NRCMs) induced cardiomyocyte enlargement and increased atrial natriuretic polypeptide (ANP) expression. Overexpression of <i>miR-139-5p</i> antagonized isoproterenol (ISO)-induced cardiomyocyte enlargement and ANP/brain natriuretic peptide (BNP) up-regulation. More importantly, we found that c-Jun expression was inhibited by <i>miR-139-5p</i> in NRCMs. Knockdown of c-Jun expression significantly attenuated cardiac hypertrophy induced by <i>miR-139-5p</i> deprivation. Our data indicated that <i>miR-139-5p</i> was down-regulated in the hearts of HCM patients and that it inhibited cardiac hypertrophy by targetting c-Jun expression.