Expression of MicroRNA-29 and Collagen in Cardiac Muscle after Swimming Training in Myocardial-Infarcted Rats

Abstract

Background: Myocardial infarction (MI) is accompanied by cardiac growth, increased collagen deposition, cell death and new vascularization of the cardiac tissue, which results in reduced ventricular compliance. The MiRNA-29 family (29a, 29b, and 29c) targets mRNAs that encode collagens and other proteins involved in fibrosis. In this study we assessed the effects of swimming training (ST) on expression of the cardiac miRNA-29 family and on genes encoding collagen after MI in rats. Methods: ST consisted of 60 min/day/10 weeks and began four weeks after MI. MiRNA and collagen expression analysis were performed in the infarcted region (IR), border region (BR) of the infarcted region and in the remote myocardium (RM) of the left ventricle. Results: MiRNA-29a expression increased 32% in BR and 52% in RM in the TR-INF compared with SED-INF. MiRNA-29c increased by 63% in BR and 55% in RM in TR-INF compared with SED-INF group. COL IAI and COL IIIAI decreased by 63% and 62% in TR-INF, respectively, compared with SED-INF. COLIIIAI expression decreased by 16% in TR-INF compared with SED-INF. Conclusion: Altogether, our results showed that ST restores cardiac miRNA-29 (a and c) levels and prevents COL IAI and COL IIIAI expression in BR and RM, which may contribute to the improvement in ventricular function induced by swimming training, after MI.

Aerobic exercise training promotes physiological cardiac remodeling involving a set of microRNAs

“…On the other hand, low levels of miRNA-29 were previously associated with fibrosis in myocardial infarction (95d). Recently, Melo et al (65) showed that swimming training restored cardiac miRNA-29a and -29c levels and prevented collagen type I and III expression on the border and in the remote regions of the myocardial infarction, suggesting the cardiac effect of exercise training in myocardial-infarcted rats as a way to prevent or minimize the harmful effects in CVD.…”

“…In contrast, exercise training-induced physiological cardiac hypertrophy presents cardioprotective effects and is not related to heart failure (74). Exercise training has been described as being able to counteract structural and functional cardiac changes in CVD by contributing to the phenotypical changes of pathological into physiological cardiac hypertrophy (31,65,73,74).…”

Long-Term Low Intensity Physical Exercise Attenuates Heart Failure Development in Aging Spontaneously Hypertensive Rats

“…In stable chronic heart failure, clinical studies have shown that long-term moderate physical training attenuates abnormal cardiac remodeling and improves functional capacity and quality of life [10,11,12,13]. In different cardiac injury models, exercise has been shown to attenuate left ventricular dilation, myocyte hypertrophy, myocardial fibrosis, mitochondrial dysfunction, myocyte calcium handling changes, sympathoexcitation, cardiac dysfunction, and improve inflammatory profile [14,15,16,17,18,19,20,21,22]. …”

The Role of MicroRNAs in the Cardiac Response to Exercise

“…We also found that miR-29c was increased in two distinct exercise models . Consistently, Souza and Melo and colleagues found that the decrease in miR-29 (a and c) seen in failing rat hearts was attenuated by aerobic exercise training, resulting in decreased collagen expression (Melo et al 2014;Souza et al 2015) and suggesting that exercise-induced miR-29 could help mitigate fibrosis and thereby improve ventricular function. We found that overexpression of miR-222, which is also upregulated in two distinct exercise models, inhibited cardiac fibrosis by three-to fourfold after IRI .…”

“…Of note, miR-222 was upregulated in both HF groups (Souza et al 2015). Other miRNAs, including miR-1, -29, -126, and -214, have also been reported to change in both healthy and diseased hearts after exercise (da Silva et al 2012;Melo et al 2014Melo et al , 2015aZhao 2015). Given limited access to tissue, there are no clinical studies to date examining human cardiac miRNA alterations after exercise.…”