Proliferative aspects of airway smooth muscle.

摘要: Increased airway smooth muscle (ASM) mass is perhaps the most important component of wall remodeling process in asthma. Known mediators ASM proliferation cell culture models fall into 2 categories: those that activate receptors with intrinsic receptor tyrosine kinase activity and have their effects through linked to heterotrimeric guanosine triphosphate-binding proteins. The major candidate signaling pathways activated by mitogens are dependent on extracellular signal-regulated phosphoinositide 3'-kinase. Increases may also involve migration, culture, key mechanisms been identified as p38 mitogen-activated protein p21-activated 1 pathways. New evidence from an vivo rat model indicates primed CD4(+) T cells sufficient trigger epithelial after allergen challenge. Hyperplasia has observed equine asthma account for increase mass. Reduction rate apoptosis play a role. beta(2)-Adrenergic agonists glucocorticoids antiproliferative against broad spectrum mitogens, although it become apparent differentially sensitive. Culture collagen type I shown enhance proliferative prevent inhibitory effect glucocorticoids, whereas beta(2)-agonists minimally affected. There no long-acting more effective than short-acting agonists, but persistent stimulation beta(2)-adrenergic probably helps suppress growth responses. maximum response fluticasone propionate thrombin-induced increased when combined salmeterol.