Disrupting actin-myosin-actin connectivity in airway smooth muscle as a treatment for asthma?

Tera L. Lavoie, Maria L. Dowell, Oren J. Lakser, William T. Gerthoffer, Jeffrey J. Fredberg, Chun Y. Seow, Richard W. Mitchell, Julian Solway*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)295-300
Number of pages6
JournalProceedings of the American Thoracic Society
Issue number3
StatePublished - May 1 2009


  • Actin
  • Asthma
  • Bronchoconstriction
  • Contractile
  • Myosin

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine


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