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1 Physiology and Cell Biology, The Ohio State University, Columbus, OH, USA
2 Molecular and Cellular Physiology, University of Cincinnati College of Medicine, Cincinnati, OH, USA
3 Pharmacology,Molecular Physiology and Biophysics, University of Vermont, Burlington, VT, USA
* To whom correspondence should be addressed. E-mail: periasamy.1{at}osu.edu.
We previously have generated an isoform-specific gene knockout mouse in which SM-B 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. 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 in wildtype animals. Calponin and activated mitogen activated protein kinase expression is increased and caldesmon expression is decreased in aorta, as well as in bladder. LC17b isoform 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.
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