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Am J Physiol Heart Circ Physiol 250: H333-H341, 1986;
0363-6135/86 $5.00
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AJP - Heart and Circulatory Physiology, Vol 250, Issue 3 333-H341, Copyright © 1986 by American Physiological Society

ARTICLES

Differential effect of thyroxine on atrial and ventricular isomyosins in rats

J. L. Samuel, L. Rappaport, I. Syrovy, C. Wisnewsky, F. Marotte, R. G. Whalen and K. Schwartz

Two myosin heavy chains (MHCs), alpha and beta, which exhibit different levels of ATPase activity related to the different velocities of muscle shortening, are differentially expressed in rat cardiac ventricles, depending on the developmental stage and the thyroid status of the animals. In contrast, no changes have been reported concerning the expression of atrial MHCs in the same physiological and pathological conditions. We have now performed studies with sensitive techniques to test the hypothesis that the expression of alpha- and beta-MHCs can also be modulated in the rat atria, although at a low level. Atrial and ventricular isomyosin patterns of various groups of rats were examined by two-dimensional peptide mapping, immunofluorescence with specific anti-alpha- and anti-beta-MHC immunoglobulins, and electrophoresis under nondenaturing conditions. Normal ontogenic development of the atria is characterized by the disappearance of a small amount of beta-MHC, present at 19 days in utero. At 3 wk of age, atria and ventricles both contain only alpha-MHC. Severe hypothyroidism, produced either by methylthiouracil (MTU) treatment of pregnant females and of their litters or by hypophysectomy of adult animals, did not significantly deinduce atrial alpha-MHC but was characterized by a significant although slight accumulation of beta-MHC (less than 5% of total myosin). This latter effect was abolished by L-thyroxine restoration. It is concluded that alpha- and beta-MHC are developmentally and hormonally regulated both in atria and ventricles, although the extent of regulation is very different for the two tissues.


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Regulation of antisense RNA expression during cardiac MHC gene switching in response to pressure overload
Am J Physiol Heart Circ Physiol, June 1, 2006; 290(6): H2351 - H2361.
[Abstract] [Full Text] [PDF]


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