Key result
Growth hormone increases skeletal muscle MRF4 expression ~94% and normalizes MyoD in heart failure rats.
Why the study?
The effects of growth hormone administration on protein expression related to skeletal muscle regulation in aortic stenosis-induced heart failure were evaluated.
Does growth hormone administration alter protein expression of myostatin, follistatin, and myogenic regulatory factors in skeletal muscle of rats with aortic stenosis-induced heart failure?
Does growth hormone administration alter protein expression of myostatin, follistatin, and myogenic regulatory factors in skeletal muscle of rats with aortic stenosis-induced heart failure?
Answers are grounded in this paper and cite their sources.
In a rat model of heart failure, growth hormone administration alters skeletal muscle myogenic regulatory factors by increasing MRF4 and normalizing MyoD expression, without affecting the myostatin/follistatin pathway.
In this study we evaluated the effects of growth hormone (GH) administration on protein expression of myostatin, follistatin, and the myogenic regulatory factors in skeletal muscle of rats with ascending aortic stenosis‐induced heart failure. Methods Male Wistar rats were subjected to thoracotomy to induce aortic stenosis (AS). After developing tachypnea/labored respiration, rats were subjected to echocardiogram and assigned to three groups (n=8): Sham, AS, and AS treated with GH (AS‐GH, 2 mg/kg/day) for 14 days. After treatment, rats were subjected to echocardiogram and euthanatized. Protein expression was evaluated by Western‐blot. Statistical analysis Anova and Tukey. Results Before GH treatment, cardiac parameters did not differ between AS and AS‐GH groups. GH preserved body weight. Right ventricular weight/BW ratio and left ventricular posterior wall thickness were higher in both AS groups than Sham. MyoD was higher in AS than Sham and similar between AS‐GH and Sham (Sham 1.0±1.3; AS 1.7±1.4; AS‐GH 1.2±1.2 arbitrary units). MRF4 expression was higher in AS‐GH than Sham (Sham 1.0±0.7; AS 1.6±0.4; AS‐GH 3.1±1.6 arbitrary units). Myostatin, follistatin, and myogenin expression did not differ between groups. Conclusion Growth hormone increases MRF4 and normalizes MyoD expression in skeletal muscle of heart failure rats. Myostatin/follistatin pathway is not changed in this experimental model.
No takes yet. Share an insight, caveat, or question.
Lima et al. (2013) studied Aortic stenosis-induced heart failure (n=24). Growth hormone vs. Sham and untreated aortic stenosis (AS) was evaluated on Protein expression of myostatin, follistatin, and myogenic regulatory factors. Growth hormone administration (2 mg/kg/day for 14 days) increased MRF4 expression (3.1 vs 1.6 arbitrary units) and normalized MyoD expression in skeletal muscle of rats with heart failure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: