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Articles in PresS, published online ahead of print October 22, 2001
Am J Physiol Cell Physiol, 10.1152/ajpcell.00390.2001
Submitted on August 10, 2001
Accepted on October 19, 2001
1 Anatomy, University of British Columbia, Vancouver, BC, Canada; St. Paul's Hospital/Providence Health Care, The UBC McDonald Research Laboratories/The iCAPTURE Center, Vancouver, BC, Canada
2 Pathology and Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada; Anatomy, University of British Columbia, Vancouver, BC, Canada; St. Paul's Hospital/Providence Health Care, The UBC McDonald Research Laboratories/The iCAPTURE Center, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: cseow{at}interchange.ubc.ca.
Myosin thick filaments have been shown to be structurally labile in intact smooth muscles. Although the mechanism of thick filament assembly/disassembly for purified myosins in solution have been well described, regulation of thick filament formation in intact muscle is still poorly understood. The present study investigates the effect of resting calcium level on thick filament maintenance in intact airway smooth muscle, and thick filament formation during activation. Cross-sectional density of the thick filaments measured electronmicroscopically showed that the density increased substantially (144%) when the muscle was activated. The abundance of filamentous myosins in relaxed muscle was calcium sensitive; in the absence of calcium (with EGTA), the filament density deceased by 35%. Length oscillation imposed on the muscle under zero-calcium condition produced no further reduction in the density. Isometric force and filament density recovered fully after re-incubation of the muscle in normal physiological saline. The results suggest that in airway smooth muscle filamentous myosins exist in equilibrium with monomeric myosins; muscle activation favors filament formation and the resting calcium level is crucial for preservation of the filaments in the relaxed state.
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