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1 Gazes Cardiac Research Institute, Cardiology Division, Medical University of South Carolina, Charleston, SC, USA
2 Division of Molecular Cardiovascular Biology, Children's Hospital Research Foundation, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: cooperge{at}musc.edu.
In large mammals there is a correlation between microtubule network densification and contractile dysfunction in severe pressure overload hypertrophy. In small mammals there is a similar correlation for the shift to 
-MHC, a MHC isoform having a slower ATPase Vmax. In this study, murine LV pressure overload invoked both mechanisms: microtubule network densification and -MHC expression. Cardiac -MHC was also augmented without altering tubulin levels by two load-independent means, chemical thyroidectomy and transgenesis. In hypertrophy, contractile function of the LV and its cardiocytes decreased proportionally; microtubule depolymerization restored normal cellular contraction. In hypothyroid mice having a complete shift from 
-MHC to -MHC, contractile function of the LV and its cardiocytes also decreased, but microtubule depolymerization had no effect on cellular contraction. In transgenic mice having a cardiac -MHC increase similar to that in hypertrophy, contractile function of the LV and its cardiocytes was normal, and microtubule depolymerization had no effect. Thus, while both mechanisms may cause contractile dysfunction, for the extent of MHC isoform switching seen even in severe murine LV pressure overload hypertrophy, microtubule network densification appears to have the more important role.
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