Abstract 2224 The Rap1 GTPase mediates fibrotic gene expression and matrix remodeling in cardiac fibroblasts

Asthma is a chronic respiratory condition characterized by airway inflammation, remodeling, and hyperresponsiveness.Estrogen has previously been shown to be responsible for the sex-oriented differences in morbidity, severity, and therapeutic responses of asthma in clinical studies.Recent data suggests that estrogen receptors (ERs), are crucial in asthma pathogenesis, but more research is needed on their exact expressions, effects, and mechanisms.The goal of this study was to gather preliminary data to support the hypothesis that estrogen exacerbates the effects of asthma via the mitogen-activated protein kinase (MAPK) pathway in human bronchial epithelial cells (BEAS-2B).BEAS-2B cells were treated with platelet derived growth factor, 17b-estradiol, and/or an ERb-agonist, with or without the presence of extracellular signal-regulated kinase (ERK) pathway inhibitors U0126 (MAPK Kinase/MEK) or BVD-523 (ERK).Proliferation, viability assays, and immunoassays, were used to analyze the effects of these treatments on the MAPK pathway and its influence on the bronchial epithelial cell proliferation.