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Myostatin expression in ventricular myocardium in a rat model of volume-overload heart failure
Insights
In volume-overload heart failure, myocardial myostatin (a protein) increases. Carvedilol treatment limits this increase in the failing heart, suggesting a therapeutic target.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Heart Failure Pathophysiology
Background:
- Mechanical stress is known to increase myocardial myostatin expression.
- Myostatin's role in chronic heart failure due to volume-overload and its modulation by beta-blockers remains largely unknown.
- This study investigates myostatin's involvement in volume-overload-induced heart failure.
Purpose of the Study:
- To investigate the expression of myostatin in the myocardium during volume-overload heart failure.
- To determine the effect of carvedilol treatment on myostatin expression in this model.
Main Methods:
- Volume-overload heart failure was induced in rats via an aorto-caval shunt over 4 weeks.
- Changes in heart weight, ventricular dimensions, and myostatin (protein and mRNA) levels were assessed.
- Effects of carvedilol, N-acetylcysteine, and doxazosin were evaluated.
Main Results:
- Shunting significantly increased heart weight, ventricular dimensions, and myocardial/skeletal myostatin levels (protein and mRNA).
- Carvedilol treatment reversed these changes, normalizing heart weight, ventricular dimensions, and myostatin expression.
- Other agents like N-acetylcysteine and doxazosin showed partial effects on myostatin expression.
Conclusions:
- Myocardial myostatin mRNA and protein expression are upregulated in a rat model of volume-overload heart failure.
- Carvedilol treatment effectively limits the increase in myostatin expression within the failing ventricular myocardium.
Background:
Mechanical stress increases myocardial myostatin expression. However, the expression of myostatin in chronic heart failure resulting from volume-overload and after treatment with beta-blockers is little known. The authors hypothesize that myostatin plays a role in the failing myocardium because of volume-overload.
Materials And Methods:
Aorto-caval shunt was created over a 4-week period in adult Sprague-Dawley rats to induce volume-overload heart failure.
Results:
Heart weight and body weight ratio significantly increased after shunting. The left ventricular end-diastolic dimension also significantly increased. Treatment with carvedilol in the shunt group reversed the increase in heart weight and ventricular dimension to the baseline values. Myocardial and skeletal myostatin proteins were up-regulated in the shunt group. The mRNA of myocardial myostatin also increased in the shunt group. Treatment with carvedilol reversed both protein and mRNA of myocardial myostatin to the baseline values. Treatment with N-acetylcysteine and doxazosin partially decreased myostatin mRNA and protein expression as compared with the shunt group. Carvedilol normalized the increased immunohistochemical labelling of myocardial myostatin in the shunt group.
Conclusion:
Myocardial myostatin mRNA and protein expression were up-regulated in the rat model of volume-overload heart failure. Treatment with carvedilol is associated with a limitation of increased myostatin expression in the failing ventricular myocardium.
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