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Research
Our group has focused on delineation of mechanisms that regulate repair of the conducting airway epithelium. We previously identified two distinct tissue specific stem cell populations that maintain the proximal and distal epithelium. Current research investigates divergent roles for the wnt/β-catenin signaling pathway in regulation of cell fate determination in these stem cell hierarchies. Our studies concentrate on analuysis of epithelial proliferation, differentiation, and migration. We make extensive use of genetically modified animal models and in vitro cell culture systems to investigate normal reparative processes and to identify processes that cause deviation from the norm. Our work and that of others indicates that the conducting airway epithelium serves as the first line of defense against environmental agents including pathogens, oxidant gases, particles, and pollutants. The normal epithelium detects, detoxifies, and eliminates such agents resulting in maintenance of an protective barrier. An attenuated or inappropriate response of the airway to such agents is associated with establishment and progression of chronic lung disease. Our analysis of epithelial protective and repair mechanisms indicates that such processes mature during the postnatal period and have led to the concept that gene-environment interactions that compromise epithelial reparative capacity are a common feature of lung diseases including bronchopulmonary dysplasia (BPD), asthma, and chronic obstructive pulmonary disease (COPD). Through interactions with basic and physician scientists at National Jewish and the University of Colorado Health Science Center, we are applying our knowledge of epithelial maintenance and repair to understanding disease etiology and development of cell based therapy for chronic lung disease. Selected Publications
Reynolds, S.D., Giangreco, A., Power, J.H.T., and Stripp, B.R., Neuroepithelial bodies of pulmonary airways serve as a reservoir of progenitor cells capable of epithelial regeneration. (2000) Am. J. Path. 156:269. Hong, K.U.*, Reynolds, S.D.*, Giangreco, A., Hurley, C. and Stripp, B.R. CCSP-expressing Cells of the Airway Neuroepithelial body Microenvironment Include a Label Retaining Subset and are Critical for Epithelial Renewal Following Progenitor Cell Depletion. (2001) Am. J. Cell Respir. Cell Mol. Biol. 24:671 (* authors contributed equally) Giangreco A. Reynolds SD. Stripp BR. Terminal bronchioles harbor a unique airway stem cell population that localizes to the bronchoalveolar duct junction. American Journal of Pathology. 161(1):173-82, 2002 Reynolds SD, Giangreco A, Hong KU, McGrath KE, Ortiz LA, Stripp BR, Airway injury in the pathophysiology of lung disease: Selective depletion of airway stem and progenitor cells potentates inflammation and alveolar dysfunction. Am J Physiol - Lung Cell Mol Physiol. 2004, 286:L1256 Hong KU, Reynolds SD, Watkins S, Fuchs E, Stripp BR: Basal cells are a multipotent progenitor capable of renewing the bronchial epithelium. Am J Pathol 2004, 164:577-588 Reynolds SD, Zemke AC, Giangreco A, Brockway, BL, Teisanu RM, Mariani TJ, Di YP, Taketo, MM, Stripp BR. Conditional stabilization of β-catenin expands the pool of lung stem cells. (in press, Stem Cells) |
Faculty
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