Exercise training in rats induced left ventricular hypertrophy that correlated with decreased GSK-3β protein activity (r=-0.70, P<0.01) and increased tissue ET-1 concentration (r=0.52, P<0.05).
Physiological exercise-induced LV hypertrophy in rats shares some molecular mechanisms with pathological hypertrophy (e.g., GSK-3β, Cain, ET-1) but differs in others (e.g., BNP, ACE).
Absolute Event Rate: 0% vs 0%
Abstract Aims: Exercise training causes physiological cardiac hypertrophy, which acts to enhance cardiac function during exercise. However, the underlying molecular mechanisms are unclear. We investigated gene expression profile of exercise training‐induced cardiac hypertrophy using left ventricle (LV) excised from exercise‐trained and sedentary control rats (12‐week old). Method: Rats in the training group exercised on a treadmill for 8‐week. Results: Left ventricular mass index and wall thickness in the exercise‐trained group were significantly greater than that in the control group, indicating that the trained rats developed cardiac hypertrophy. Of the 3800 genes analysed in the microarray analyses, a total of 75 relevant genes (upregulation of 33 genes and downregulation of 42 genes) displayed alterations with exercise training. Among these genes, we focused on glycogen synthase kinase (GSK)‐3 β , calcineurin‐inhibitor (Cain), and endothelin (ET)‐1 for their implicated roles in pathological cardiac hypertrophy, and confirmed the results of microarray analysis at mRNA and protein/peptide levels using quantitative PCR, Western blot, and EIA analyses. The gene expression of GSK‐3 β decreased significantly and those of Cain and ET‐1 increased significantly with exercise training. Furthermore, LV mass index was significantly correlated with GSK‐3 β protein activity ( r = −0.70, P < 0.01) and tissue ET‐1 concentration ( r = 0.52, P < 0.05). There were no changes in gene expressions in brain natriuretic peptide (BNP), angiotensin‐correcting enzyme (ACE), interleukin‐6, and vascular cell adhesion molecule (VCAM)‐1. Conclusion: These findings suggest that physiological and pathological LV hypertrophy may share some of the same molecular mechanisms in inducing LV hypertrophy (e.g. GSK‐3 β , Cain, and ET‐1) and that other genes (e.g. BNP, ACE) may differentiate physiological from pathological LV hypertrophy.
Iemitsu et al. (Wed,) reported a other. Exercise training in rats induced left ventricular hypertrophy that correlated with decreased GSK-3β protein activity (r=-0.70, P<0.01) and increased tissue ET-1 concentration (r=0.52, P<0.05).