Methacholine-induced airway hyperresponsiveness is dependent on Gαq signaling

Michael T. Borchers, T. Biechele, J. P. Justice, T. Ansay, S. Cormier, V. Mancino, T. M. Wilkie, M. I. Simon, N. A. Lee, J. J. Lee

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


Airway function in health and disease as well as in response to bronchospastic stimuli (i.e., irritants, allergens, and inflammatory mediators) is controlled, in part, by cholinergic muscarinic receptor regulation of smooth muscle. In particular, the dependence of airway smooth muscle contraction/relaxation on heterotrimeric G protein-coupled receptor signaling suggests that these events underlie the responses regulating airway function. Gαq-containing G proteins are proposed to be a prominent signaling pathway, and the availability of knockout mice deficient of this subunit has allowed for an investigation of its potential role in airway function. Airway responses in Gαq-deficient mice (activities assessed by both tracheal tension and in vivo lung function measurements) were attenuated relative to wild-type controls. Moreover, ovalbumin sensitization/aerosol challenge of Gαq-deficient mice also failed to elicit an allergen-induced increase in airway reactivity to methacholine. These findings indicate that cholinergic receptor-mediated responses are dependent on Gαq-mediated signaling events and identify Gαq as a potential target of preventative/intervening therapies for lung dysfunction.

Original languageEnglish (US)
Pages (from-to)L114-L120
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number1 29-1
StatePublished - Jul 1 2003


  • G protein
  • Gene knockout mice

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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