Increased expression of G.ALPHA.q protein in bronchial smooth muscle of mice with allergic bronchial asthma

Abstract

In the present study, the change in Gq protein level in bronchial smooth muscle of mice with antigen-induced airway hyperresponsiveness (AHR) was determined. BALB/c mice were actively sensitized and repeatedly challenged with ovalbumin antigen to induce bronchial smooth muscle hyperresponsiveness. The contraction induced by 10 µM AlF4-(generated by 10 µM AlCl3 plus 10 mM NaF) of bronchial smooth muscles isolated from the antigen-challenged mice was significantly augmented as compared with that from the control animals. The Gαq protein level determined by immunoblotting was also significantly increased in bronchial smooth muscles of the antigen-challenged group. Thus, an upregulation of Gαq protein may be involved in the pathogenesis of bronchial smooth muscle hyperresponsiveness, one of the causes of AHR in asthmatics.

Targeted inhibition of G q signaling induces airway relaxation in mouse models of asthma

“…The individual or combined activation of many of these receptors induces an increase in airway resistance, which is the hallmark of airway hyperresponsiveness (1). In addition, increased expression of G q and G i proteins has been reported in animal models of asthma (2,3). Elevated G q -coupled receptor agonists such as acetylcholine, thromboxane, or histamine have also been found in the airways of patients with asthma (4).…”