The role of microRNA‐208a in cardiac hypertrophy induced by aerobic physical training

The miRNA‐208 regulates gene expression of slow myosin heavy chain(MHC)in heart. We investigated the role of miRNA‐208 and its target Thyroid Hormone Receptor Associated Protein 1 (THRAP1) in aerobic training (AT) induced cardiac hypertrophy (CH). Female Wistar Rats(n=21)into 3 groups: sedentary (S), Trained 1(T1): swimming sessions of 60′, 5 days/week (10 weeks). Trained 2(T2): similar to T1 until 8th week, on the 9th week the rats swan twice/day and on the 10th week 3 times/day. Were assessed: heart rate (HR), blood pressure (BP) by direct measurement, VO2max by ergoespirometry, soleus citrate synthase (CS) activity by spectrophotometer, ventricular function and CH by echocardiography (EGC), CH by LV/BW ratio (mg/g) and cardiomyocyte diameter (CD), gene expression of atrial natriuretic factor (ANF), skeletal α‐actin, α‐MHC and β‐MHC and miR‐208 by Real‐time PCR and protein content of α and β‐MHC and THRAP1 by Western Blott. AT decreased HR and increased VO2max (11%/T1 and 15%/T2) and CS (47%/T1 and 105%/T2). LV/BW ratio increased 13%/T1 and 28%/T2 and CD increased 20%/T1 and 30%/T2. Gene expression of skeletal α‐actin decreased 53%/T2. The E/A ratio increased and isovolumetric relaxation time and myocardial performance index decreased. MiR‐208 expression decreased 62%/T2 with a decrease of β‐MHC and an increase of α‐MHC gene expression(β/‐71%,α/+37%) and protein content(β/−45 % α/+72%) in T2. THRAP1 protein increased 40%/T2 compared with S. APT induced physiological CH and improved diastolic function. MiR‐208a and β‐MHC expression decreased and THRAP‐1 increased. The decrease of miR‐208 was opposite to disease and can be a therapeutic strategy in pathological CH. Support: FAPESP/CAPES/NIH