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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Left ventricular isomyosins in normal and hypertrophied rat and human hearts.

Regulation of rat cardiac contractility by changes in the expression of a particular form of myosin (V1-V3) has been demonstrated with a pressure overload. Previous reports of the effect of a volume overload have been controversial. Therefore, we measured the isomyosin composition and mechanical function in the same papillary muscles from rat hearts subjected to a chronic volume overload (aortic insufficiency, AI). A marked change in isomyosin composition from V1 to V3 occurred. Contractility, as assessed by shortening velocity Vmax, was also significantly decreased, and this decrease was correlated with the isomyosin transformation. The changes in isomyosin composition and speed of contraction with AI are thus similar to changes induced by aortic stenosis. Little experimental evidence exists for involvement of such changes in the regulation of human cardiac contractility. Using immunoglobulins highly specific for V1 and V3 in autopsy samples we have observed that the human left ventricle is mostly composed of a V3 isoform (HV3) and that small amounts (1 to 15%) of a V1 type ( HV1) are present in foetal and some adult hearts. This HV1 is absent from the left ventricles of patients with valvular disease, assessed at the time of valve replacement (N = 30, samples provided by Dr P. Menasché). Myosin Ca2+- stimulated ATPase activities were not significantly different between normal and hypertrophied hearts. These data demonstrate the heterogeneity of human ventricular myosin, which is composed of V1 and V3 isomyosins, as in other mammalian species. Isomyosin shifts from V1 to V3 are possible in man, but they are quantitatively small and without noticeable influence on overall ATPase activities.[1]


  1. Left ventricular isomyosins in normal and hypertrophied rat and human hearts. Schwartz, K., Apstein, C., Mercadier, J.J., Lecarpentier, Y., de la Bastie, D., Bouveret, P., Wisnewsky, C., Swynghedauw, B. Eur. Heart J. (1984) [Pubmed]
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