Abstract
Asthma is a disease characterized by inflammation, airway remodeling, and increased bronchial smooth muscle (BSM) tone. In BSM, stimulation of Gq-coupled receptors linked to numerous procontractile ligands activates PLCβ, which in turns leads to efflux of Ca2+ stores from endoplasmic reticulum into the cytoplasm. The accumulated cytosolic Ca2+ activates myosin light chain kinase (MLCK), which promotes actin-myosin interaction and smooth muscle cell contraction. Regulator of G protein signaling (RGS) proteins act as a GTPase accelerating proteins (GAPs) to terminate Gq and Gi-mediated signaling pathways.
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