Isoform switching from SM-B to SM-A myosin results in decreased contractility and altered expression of thin filament regulatory proteins

We previously generated an isoform-specific gene knockout mouse in which SM-B myosin is permanently replaced by SM-A myosin. In this study, we examined the effects of SM-B myosin loss on the contractile properties of vascular smooth muscle, specifically peripheral mesenteric vessels and aorta. The a...

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Bibliographic Details
Published in:American Journal of Physiology: Cell Physiology 2004-09, Vol.56 (3), p.C723-C729
Main Authors: BABU, Gopal J, PYNE, Gail J, YINGBI ZHOU, OKWUCHUKUASANYA, Chris, BRAYDEN, Joseph E, OSOL, George, PAUL, Richard J, LOW, Robert B, PERIASAMY, Muthu
Format: Article
Language:English
Subjects:
Biological and medical sciences
Cell physiology
Cells
Circulatory system
Coronary vessels
Fundamental and applied biological sciences. Psychology
Molecular and cellular biology
Muscle contraction
Muscular system
Proteins
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Summary:We previously generated an isoform-specific gene knockout mouse in which SM-B myosin is permanently replaced by SM-A myosin. In this study, we examined the effects of SM-B myosin loss on the contractile properties of vascular smooth muscle, specifically peripheral mesenteric vessels and aorta. The absence of SM-B myosin leads to decreased velocity of shortening and increased isometric force generation in mesenteric vessels. Surprisingly, the same changes occur in aorta, which contains little or no SM-B myosin in wild-type animals. Calponin and activated mitogen-activated protein kinase expression is increased and caldesmon expression is decreased in aorta, as well as in bladder. Light chain-17b isoform (LC17b) expression is increased in aorta. These results suggest that the presence or absence of SM-B myosin is a critical determinant of smooth muscle contraction and that its loss leads to additional changes in thin filament regulatory proteins. [PUBLICATION ABSTRACT]
ISSN:0363-6143
1522-1563