Voluntary exercise for 3 and 6 weeks in female rats increased ventricular TGF-beta(1) mRNA expression, while prepro-ANP, TGF-beta(3), and extracellular matrix proteins remained unchanged.
Does voluntary exercise alter the mRNA expression of TGF-beta and prepro-ANP in a physiological model of cardiac hypertrophy in rats?
Physiological cardiac hypertrophy induced by exercise upregulates TGF-beta1 mRNA but not prepro-ANP, distinguishing its molecular profile from pathological hypertrophy.
The induction of transforming growth factor (TGF)-beta and prepro-atrial natriuretic peptide (ANP) mRNAs represent hallmark features of pathological cardiac hypertrophy. The present study examined whether this pattern of mRNA expression was conserved in a physiological model of cardiac hypertrophy. To address this thesis, female Sprague-Dawley rats were individually housed and permitted to run freely. Voluntary exercise for 3 and 6 wk resulted in biventricular hypertrophy and increased cytochrome c oxidase activity in the triceps muscle. In the hypertrophied left ventricle, the steady-state mRNA level of the cardiac fetal gene prepro-ANP and the extracellular matrix proteins preprocollagen-alpha(1) and fibronectin were similar in exercise-trained and sedentary rats. By contrast, an increased expression of TGF-beta(1) mRNA was observed, whereas TGF-beta(3) mRNA level was unchanged in the hypertrophied left ventricle of exercise-trained compared with sedentary rats. These data highlight a heterogeneity in the regulation of TGF-beta isoforms, and the increased expression of ventricular TGF-beta(1) mRNA in physiological cardiac hypertrophy may contribute to myocardial remodeling.
Calderone et al. (Wed,) conducted a other in Exercise-induced cardiac hypertrophy. Voluntary exercise vs. Sedentary was evaluated on mRNA expression of TGF-beta isoforms, prepro-ANP, preprocollagen-alpha(1), and fibronectin. Voluntary exercise for 3 and 6 weeks in female rats increased ventricular TGF-beta(1) mRNA expression, while prepro-ANP, TGF-beta(3), and extracellular matrix proteins remained unchanged.