In a rat model of chronic heart failure, diaphragm myosin heavy chain isoform changes are related to ventricular dysfunction severity rather than being modulated by myogenic regulatory factors.
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Diaphragm MyHC shifts track HF severity independent of MRFs in rats; human relevance and mechanisms remain open.
Objective In this study we tested the hypothesis that diaphragm myosin heavy chain (MyHC) isoform changes are related to alterations of myogenic regulatory factors (MRF) expression in chronic heart failure. Methods We studied Sham (n=10) and infarcted rats with heart failure (MI/HF, n=10). Cardiac structures and ventricular function were assessed by echocardiogram. MyHC isoforms were analyzed by electrophoresis. MRF myogenin, MyoD, and MRF4 gene expression was evaluated by real time RT‐PCR and protein expression was analyzed by Western‐blot. Statistical analysis was performed by Student's t test and Pearson correlation. Results All MI/HF rats had pulmonary congestion and right ventricular hypertrophy. In echocardiographic evaluation, MI/HF presented left cardiac chambers dilation and left ventricular systolic and diastolic dysfunction. The percentage of MyHC I isoform was higher and IIb isoform was lower in MI/HF. Left atrial diameter‐to‐body weight ratio positively correlated with MyHC I and negatively correlated with MyHC IIb isoform percentage. No differences were observed in MRF gene and protein expressions between groups. Conclusion MRF expression does not modulate diaphragm MyHC isoforms changes in rats with chronic heart failure. Diaphragm MyHC changes are related to ventricular dysfunction severity. Financial support: Fapesp.
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Lima et al. (2011) studied this question.
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