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Published on: July 26, 2018
Myostatin and follistatin expression in skeletal muscles of rats with chronic heart failure
Aline Regina Ruiz Lima1, Paula Felippe Martinez, Katashi Okoshi
1Department of Internal Medicine, Botucatu Medical School, State University of Sao Paulo-UNESP, Botucatu, Sao Paulo, Brazil.
Abstract:
Skeletal muscle abnormalities can contribute to decreased exercise capacity in heart failure. Although muscle atrophy is a common alteration in heart failure, the mechanisms responsible for muscle mass reduction are not clear. Myostatin, a member of TGF-beta family (transforming growth factor), regulates muscle growth and mass. Several studies have shown a negative correlation between myostatin expression and muscle mass. The aim of this study was to evaluate myostatin expression in skeletal muscles of rats with heart failure. As myostatin gene expression can be modulated by follistatin, we also evaluated its expression. Heart failure was induced by myocardial infarction (MI, n = 10); results were compared to Sham-operated group (n = 10). Ventricular function was assessed by echocardiogram. Gene expression was analyzed by real-time PCR and protein levels by Western blotting in the soleus and gastrocnemius muscles; fibre trophism was evaluated by morphometric analysis. MI group presented heart failure evidence such as pleural effusion and right ventricular hypertrophy. Left ventricular dilation and dysfunction were observed in MI group. In the soleus muscle, cross-sectional area (P = 0.006) and follistatin protein levels (Sham 1.00 +/- 0.36; MI 0.18 +/- 0.06 arbitrary units; P = 0.03) were lower in MI and there was a trend for follistatin gene expression to be lower in MI group (P = 0.085). There was no change in myostatin expression between groups. In gastrocnemius, all MI group parameters were statistically similar to the Sham. In conclusion, our data show that during chronic heart failure, decreased skeletal muscle trophism is combined with unchanged myostatin and reduced follistatin expression.
Insights
Heart failure in rats reduced skeletal muscle size and follistatin protein levels, but did not alter myostatin expression. This suggests follistatin, not myostatin, may be involved in heart failure-related muscle loss.
Area of Science:
- Cardiovascular Research
- Skeletal Muscle Physiology
- Molecular Biology
Background:
- Skeletal muscle abnormalities contribute to reduced exercise capacity in heart failure.
- Muscle atrophy is common in heart failure, but the underlying mechanisms remain unclear.
- Myostatin, a TGF-beta family member, regulates muscle growth and mass, with inverse correlation to muscle mass.
Purpose of the Study:
- To investigate myostatin and follistatin expression in skeletal muscles of rats with heart failure.
- To determine the relationship between myostatin/follistatin and muscle mass changes in heart failure.
Main Methods:
- Heart failure induced by myocardial infarction (MI) in rats, compared to Sham-operated controls.
- Assessed ventricular function via echocardiogram.
- Analyzed gene expression (real-time PCR) and protein levels (Western blotting) in soleus and gastrocnemius muscles.
- Evaluated muscle fiber trophism using morphometric analysis.
Main Results:
- MI group exhibited heart failure signs, including pleural effusion and right ventricular hypertrophy, with left ventricular dilation and dysfunction.
- Soleus muscle showed reduced cross-sectional area and significantly lower follistatin protein levels in the MI group.
- A trend towards lower follistatin gene expression was observed in the MI group's soleus muscle.
- No significant changes in myostatin expression were found in either muscle group.
- Gastrocnemius muscle parameters remained similar between MI and Sham groups.
Conclusions:
- Chronic heart failure in rats is associated with decreased skeletal muscle trophism.
- Reduced follistatin expression, but not myostatin, accompanies muscle atrophy in this heart failure model.
- Follistatin may play a role in the skeletal muscle abnormalities observed in heart failure.
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