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Transforming growth factor- induces fibrosis in immune cell-depleted lungs Mitchell A. Olman 1 ,2 and Michael A. Matthay 3 Departments of 1 Medicine and 2 Pathology, Division of Pulmonary and Critical Care Medicine, University of Alabama, Birmingham, Alabama 35294; and the 3 Cardiovascular Research Institute, University of California at San Francisco, San Francisco, California 94145 THE STUDY by Xu and colleagues, one of the current articles in focus (Ref. 30a , see p. L527 in this issue), addresses the potential role of epithelial cell production of transforming growth factor (TGF)- on fibrosis using immune cell-depleted lung tissue slices. This question is important because activation of TGF- through interaction with the protease cleavage, binding to the matricellular protein thrombospondin-cell surface receptor CD36 complex, or the epithelial-specific integrin α v 6 may result in temporally and spatially restricted TGF- to sites of injury. If epithelial-specific activation pathways are found to be dominant, they could be modulated with therapeutic intent. Fibroblast epithelial cell interactions in fibrosis. The in vivo and in vitro studies of Adamson et al. ( 2 , 3 ) and others reveal a complex interdependence of fibroblast and epithelial cells during lung injury and repair. Epithelial cells can
AJP - Lung Cellular and Molecular Physiology – The American Physiological Society
Published: Sep 1, 2003
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