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The Proceedings of the American Thoracic Society 6:295-300 (2009)
© 2009 The American Thoracic Society
doi: 10.1513/pats.200808-078RM
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Disrupting Actin-Myosin-Actin Connectivity in Airway Smooth Muscle as a Treatment for Asthma?

Tera L. Lavoie1, Maria L. Dowell2, Oren J. Lakser2, William T. Gerthoffer3, Jeffrey J. Fredberg4, Chun Y. Seow5, Richard W. Mitchell1 and Julian Solway1

Departments of 1 Medicine and 2 Pediatrics, University of Chicago, Chicago, Illinois; 3 Department of Biochemistry and Molecular Biology, University of South Alabama, Mobile, Alabama; 4 Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts; and 5 Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada

Correspondence and requests for reprints should be addressed to Julian Solway, M.D., University of Chicago, MC6026, 5841 S. Maryland Ave., Chicago, IL 60637. E-mail: jsolway{at}medicine.bsd.uchicago.edu

ABSTRACT

Breathing is known to functionally antagonize bronchoconstriction caused by airway muscle contraction. During breathing, tidal lung inflation generates force fluctuations that are transmitted to the contracted airway muscle. In vitro, experimental application of force fluctuations to contracted airway smooth muscle strips causes them to relengthen. Such force fluctuation–induced relengthening (FFIR) likely represents the mechanism by which breathing antagonizes bronchoconstriction. Thus, understanding the mechanisms that regulate FFIR of contracted airway muscle could suggest novel therapeutic interventions to increase FFIR, and so to enhance the beneficial effects of breathing in suppressing bronchoconstriction. Here we propose that the connectivity between actin filaments in contracting airway myocytes is a key determinant of FFIR, and suggest that disrupting actin-myosin-actin connectivity by interfering with actin polymerization or with myosin polymerization merits further evaluation as a potential novel approach for preventing prolonged bronchoconstriction in asthma.

Key Words: asthma • bronchoconstriction • myosin • actin • contractile






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