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Local response to cardiac overload on myosin heavy chain gene expression and isozyme transition
S Imamura1, R Matsuoka, E Hiratsuka
1Pediatric Cardiology, Heart Institute of Japan, Tokyo Women's Medical College, Japan.
Insights
Cardiac myosin heavy chain (MHC) gene expression changes during pressure overload are localized. Studies show that one-sided ventricular overload affects only the loaded ventricle, not the other.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Cardiac Remodeling
Background:
- Cardiac myosin heavy chain (MHC) gene expression shifts during pressure overload.
- The precise triggers for these shifts—intrinsic factors versus direct myocyte stress—remain unclear.
Purpose of the Study:
- To determine if cardiac MHC gene expression changes during pressure overload are confined to the overloaded ventricle.
- To investigate whether these changes extend to the unloaded ventricle.
Main Methods:
- Examined MHC gene expression and isozyme transition in both left and right ventricles of rats.
- Utilized models of one-sided ventricular pressure overload: aortic coarctation and pulmonary artery banding.
- Confirmed that pressure overload was localized to the targeted ventricle.
Main Results:
- No significant induction of beta-MHC messenger RNA or protein was observed in the unloaded ventricle.
- Significant induction of beta-MHC messenger RNA and protein occurred in the overloaded ventricle.
- Results indicate that pressure overload is indeed limited to the loaded ventricle.
Conclusions:
- Changes in cardiac MHC gene expression and isozyme transition due to one-sided ventricular overload are localized to the affected ventricle.
- Cardiac MHC gene regulation during hemodynamic overload is likely a direct local response to increased load, not induced by systemic intrinsic factors.
Abstract:
It is uncertain whether the shift of cardiac myosin heavy chain (MHC) during pressure overload can be induced by some intrinsic factors or by the stress imposed directly on the individual myocytes. To study whether the changes in cardiac MHC gene expression produced by one-sided overload are limited to the involved ventricle or extend to the other ventricle, we examined MHC gene expression and isozyme transition in the left and right ventricles in aortic coarctated and pulmonary artery-banded rats. It has been confirmed that the pressure overload is indeed limited to the loaded ventricle. The results showed that, compared with sham-operated rats, there was no significant induction of the beta-MHC messenger RNA and corresponding protein in the unloaded ventricle, whereas significant induction was observed in the overloaded ventricle. These results demonstrated that the changes in MHC gene expression and isozyme produced by one-sided ventricular overload are limited to the involved ventricle. We conclude that the MHC gene regulation during hemodynamic overload may not be induced by intrinsic factors, such as hormones, catecholamine, or atrial natriuretic peptide, but is induced by direct local response to increased load.