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Protein expression of myostatin and follistatin in the myocardium of spontaneously hypertensive rats with heart failure
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The aim of this study was to evaluate myocardial myostatin and follistatin protein expression in spontaneously hypertensive rats (SHR) with heart failure (HF).
Methods
18‐month‐old SHR's were evaluated to identify clinical features of HF: tachypnea/labored respiration and weight loss. After HF was detected, rats were subjected to transthoracic echocardiogram and euthanized. During euthanasia, we evaluated pathological evidence of HF such as pulmonary congestion and right ventricular hypertrophy. Wistar‐Kyoto (WKY) rats were used as controls. Myostatin and follistatin protein expression was assessed by Western blotting.
Results
All SHR's (n=8) presented tachypnea, lung congestion and right ventricular hypertrophy. No WKY rat (n=8) presented any feature of HF. Echocardiographic evaluation showed left chambers dilation (left atrial diameter: WKY 5.73±0.59; SHR 7.28±1.17 mm; p=0.004; left ventricular diastolic diameter/body weight ratio: WKY 19.6±3.1; SHR 27.7±4.7 mm/kg; p=0.001), and left ventricular systolic (fractional shortening: WKY 54.6±6.3; SHR 42.2±7.1 %; p=0.003) and diastolic dysfunction in SHR. Myostatin (WKY 1.00±0.16; SHR 0.77±0.23 arbitrary units; p=0.035) and follistatin (WKY 1.00±0.35; SHR 0.49±0.18 arbitrary units; p=0.002) protein expression was lower in SHR.
Conclusion
Myostatin and follistatin protein expression is reduced in myocardium of SHR with heart failure.
Title: Protein expression of myostatin and follistatin in the myocardium of spontaneously hypertensive rats with heart failure
Description:
The aim of this study was to evaluate myocardial myostatin and follistatin protein expression in spontaneously hypertensive rats (SHR) with heart failure (HF).
Methods
18‐month‐old SHR's were evaluated to identify clinical features of HF: tachypnea/labored respiration and weight loss.
After HF was detected, rats were subjected to transthoracic echocardiogram and euthanized.
During euthanasia, we evaluated pathological evidence of HF such as pulmonary congestion and right ventricular hypertrophy.
Wistar‐Kyoto (WKY) rats were used as controls.
Myostatin and follistatin protein expression was assessed by Western blotting.
Results
All SHR's (n=8) presented tachypnea, lung congestion and right ventricular hypertrophy.
No WKY rat (n=8) presented any feature of HF.
Echocardiographic evaluation showed left chambers dilation (left atrial diameter: WKY 5.
73±0.
59; SHR 7.
28±1.
17 mm; p=0.
004; left ventricular diastolic diameter/body weight ratio: WKY 19.
6±3.
1; SHR 27.
7±4.
7 mm/kg; p=0.
001), and left ventricular systolic (fractional shortening: WKY 54.
6±6.
3; SHR 42.
2±7.
1 %; p=0.
003) and diastolic dysfunction in SHR.
Myostatin (WKY 1.
00±0.
16; SHR 0.
77±0.
23 arbitrary units; p=0.
035) and follistatin (WKY 1.
00±0.
35; SHR 0.
49±0.
18 arbitrary units; p=0.
002) protein expression was lower in SHR.
Conclusion
Myostatin and follistatin protein expression is reduced in myocardium of SHR with heart failure.
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