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Methacholine-induced airway hyperresponsiveness is dependent on G_q signaling

Department of Biochemistry and Molecular Biology, ¹Division of Pulmonary Medicine, ²Division of Hematology and Oncology, Mayo Clinic Scottsdale, Scottsdale, Arizona 85259; ³Division of Biology, California Institute of Technology, Pasadena, California 91125; and ⁴Pharmacology Department, University of Texas Southwestern, Dallas, Texas 75390-9041

Submitted 25 September 2002 ; accepted in final form 24 February 2003

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. G_q-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 G_q-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 G_q-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 G_q-mediated signaling events and identify G_q as a potential target of preventative/intervening therapies for lung dysfunction.

G protein; gene knockout mice

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