MicroRNA-214 Inhibits Cardiac Remodeling in Mouse Models of Cardiac Pressure Overload

To determine the role of microRNA 214 (miR-214) on cardiac remodeling, mouse model of cardiac pressure overload induced by transverse aortic constriction (TAC) was established. Kunming mice were randomly divided into three groups: Ad-GFP group, Ad-miR-214 group and sham-surgery group. Left ventricular (LV) dimensions, HW/BW, collagen type I, type III, ANP, beta-MHC were measured. In Ad-miR-214 group, LV dimensions, HW/BW, collagen type I, type III, ANP, beta-MHC all significantly decreased compared with the Ad-GFP group. At 8 weeks after TAC surgery, the Ad-miR-214 significantly improved LVSP, LV+ dp/dt(max), LV-dp/dt(min), and decreased heart rate (HR) and LVEDP compared with Ad-GFP group. Compared with Ad-GFP, the cell apoptotic rate significantly decreased in the Ad-miR-214 group. Furthermore, mice were randomly divided into 2 groups, control group and the Ad-anti-miR group treated with or without miR-214 inhibitor. Heart failure markers and myocardial collagen type I and type III were compared, and there was no significant difference between the Ad-anti-miR group and the control group, suggesting miR-214 mutant mice have normal cardiac structure and function. In conclusion, ad-miR-214 was proven to be effective in inhibiting cardiac hypertrophy, fibrosis and decreasing the apoptosis of myocardial cells induced by cardiac pressure overload.