Effects of miR-29a and miR-101a Expression on Myocardial Interstitial Collagen Generation After Aerobic Exercise in Myocardial-infarcted Rats

Background and Aims Myocardial infarction (MI) is accompanied by increased collagen deposition, cell necrosis and angiogenesis in cardiac tissue, which results in reduced ventricular compliance. Both microRNA-29a (miR-29a) and microRNA-101a (miR-101a) target the mRNAs encoding collagens and other proteins involved in fibrosis. Methods We assessed the effects of intermittent aerobic exercise on the expression of cardiac miR-29a and miR-101a and following effects on the TGFβ, fos , Smad2/3, COL1A1 and COL3A1 in MI model of rats. Intermittent aerobic exercise for MI rats was begun from the second week and ended at the ninth week postsurgery. Expressions of microRNAs (miRNAs) and fibrosis-associated genes were detected from the infarction adjacent region located in the left ventricle. The heart coefficient (HC = heart weight/body weight) and hemodynamics assay were used to evaluate cardiac function level. Results Intermittent aerobic exercise inhibited myocardial interstitial collagen deposition and significantly improved cardiac function of MI rats. The results of real-time PCR and Western blot indicate that intermittent aerobic exercise enhanced the expression of miR-29a and miR-101a and inhibited TGFβ pathway in the MI rats. Conclusions Our results suggest that controlled intermittent aerobic exercise can inhibit TGFβ pathway via up-regulation to the expression of miR-29a and miR-101a and finally cause a reduced fibrosis and scar formation in cardiac tissue. We believe that controlled intermittent aerobic exercise is beneficial to the healing and discovery of damaged cardiac tissues and their function after MI.