Exercise training restores the cardiac microRNA-1 and −214 levels regulating Ca2+ handling after myocardial infarction

Abstract

BackgroundImpaired cardiomyocyte contractility and calcium handling are hallmarks of left ventricular contractile dysfunction. Exercise training has been used as a remarkable strategy in the treatment of heart disease. The microRNA-1, which targets sodium/calcium exchanger 1 (NCX), and microRNA-214, which targets sarcoplasmic reticulum calcium ATPase-2a (Serca2a), are involved in cardiac function regulation. Thus, the aim of this study was to evaluate the effect of exercise training on cardiac microRNA-1 and −214 expression after myocardial infarction.MethodsWistar rats were randomized into four groups: sedentary sham (S-SHAM), sedentary infarction (S-INF), trained sham (T-SHAM), and trained infarction (T-INF). Exercise training consisted of 60 min/days, 5 days/week for 10 weeks with 3 % of body weight as overload beginning four weeks after myocardial infarction.ResultsMicroRNA-1 and −214 expressions were, respectively, decreased (52 %) and increased (54 %) in the S-INF compared to the S-SHAM, while exercise training normalized the expression of these microRNAs. The microRNA targets NCX and Serca-2a protein expression were, respectively, decreased (55 %) and increased (34 %) in the T-INF group compared to the S-INF group.ConclusionsThese results suggest that exercise training restores microRNA-1 and −214 expression levels and prevents change in both NCX and Serca-2a protein and gene expressions. Altogether, our data suggest a molecular mechanism to restore ventricular function after exercise training in myocardial infarction rats.

The Role of MicroRNAs in the Cardiac Response to Exercise

“…Resistance training decreased the expression of miR-214 contributing to up-regulation of its target, SERCA2a, which enhances SR Ca 2þ -uptake accelerating cardiomyocyte relaxation and loading the SR with Ca 2þ , thereby improving peak Ca 2þ release and contractility (Melo et al 2015a). Melo et al (2015b) also found that swimming increased miR-1 (targeting NCX1) and decreased miR-214 (targeting NCX1 and SERCA2a) regulating Ca 2þ handling after MI.…”

Exercise and epigenetic inheritance of disease risk

“…Cardiac dysfunction caused by myocardial infarction is attenuated by aerobic exercise training, and seems to be controlled by miRNAs. The aberrant increased and decreased expression of miR‐214 and miR‐1, respectively, caused by surgery‐induced myocardial infarction (MI) in Wistar rats, was restored to pre‐infarct levels after forced swimming exercise . Moreover, exercise training prevented cardiac scarring and cardiac dysfunction after MI by increasing cardiac miR‐29a and miR‐29c abundance, subsequently reducing the expression of collagen gene (collagen type I alpha 1 and collagen type III alpha I) .…”

Regulation of Gene Expression by Exercise-Related Micrornas

“…Accordantly, a combinatorial expression of several miRs has been suggested to determine cardioprotective effects against hypoxia and aging [119,120]. Resistance physical exercise in Wistar rats decreases expression of miR-214 in the left ventricule that leads to increased SERCA2 expression and improved cardiac contractile function [121]. Although exercise has been reported to protect against cardiac injuries, future research are needed to define the ideal rate, duration and intensity at the physical activity can attenuate cardiovascular disease processes.…”