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J Appl Physiol 90: 1811-1816, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 5, 1811-1816, May 2001

Myosin thick filament lability induced by mechanical strain in airway smooth muscle

Kuo-Hsing Kuo1, Lu Wang2, Peter D. Paré2, Lincoln E. Ford3, and Chun Y. Seow1,4,5

Departments of 1 Anatomy and 4 Pharmacology and Therapeutics, University of British Columbia, Vancouver V6T 1Z3; 2 Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, Vancouver V6Z 1Y6; 3 Krannert Institute of Cardiology, Indiana University, Indianapolis, Indiana 46220; and 5 Department of Pathology and Laboratory Medicine, St. Paul's Hospital, University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6

Airway smooth muscle adapts to different lengths with functional changes that suggest plastic alterations in the filament lattice. To look for structural changes that might be associated with this plasticity, we studied the relationship between isometric force generation and myosin thick filament density in cell cross sections, measured by electron microscope, after length oscillations applied to the relaxed porcine trachealis muscle. Muscles were stimulated regularly for 12 s every 5 min. Between two stimulations, the muscles were submitted to repeated passive ±30% length changes. This caused tetanic force and thick-filament density to fall by 21 and 27%, respectively. However, in subsequent tetani, both force and filament density recovered to preoscillation levels. These findings indicate that thick filaments in airway smooth muscle are labile, depolymerization of the myosin filaments can be induced by mechanical strain, and repolymerization of the thick filaments underlies force recovery after the oscillation. This thick-filament lability would greatly facilitate plastic changes of lattice length and explain why airway smooth muscle is able to function over a large length range.

swine trachea; mechanics; length perturbation; plasticity


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