4.4 Article

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

Journal

BMC CARDIOVASCULAR DISORDERS
Volume 15, Issue -, Pages -

Publisher

BMC
DOI: 10.1186/s12872-015-0156-4

Keywords

Exercise training; Myocardial infarction; MicroRNA; Cardiac function

Funding

  1. FAPESP Fellowship [2010/09438-0, 2012/04104-2]
  2. CNPq-PDE Fellowship [308267/2013-3]
  3. Barauna VG CNPq-Universal [485873/2012-5]
  4. FAPESP [2009/18370-3, 2010/50048-1]

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Background: Impaired 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. Methods: Wistar 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. Results: MicroRNA-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. Conclusions: These 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.

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