TGF-BETA IN AIRWAY EPITHELIAL REPAIR

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The airway epithelium may be damaged extensively in inflammatory responses to environmental agents and allergen exposure, in part by apoptosis. Transforming growth factor-beta (TGF-b) may prevent epithelial cell apoptosis. Given the role of TGF-b in mediating both inflammation and tissue remodeling, Understanding how TGF-b protects airway epithelium is of importance. We will grow airway epithelium collected from asthmatic and normal subjects and examine differences in the protective effect of TGF-b after activation of the Fas death receptor. We will identify differences in Smad7, cell cycle, p21 and p15 expression, and cell activation that may explain the relative resistance of asthmatic epithelial cells to the protective effect of TGF-b. These studies should provide important new insights into a fundamental mechanism controlling airway epithelial homeostasis. Understanding the process may suggest new therapeutic interventions to protect the airway epithelium form damage in asthma.