title: Role for alpha3 integrin in EMT and pulmonary fibrosis.
abstract: Idiopathic pulmonary fibrosis (IPF) is characterized by progressive (myo)fibroblast accumulation and collagen deposition. One possible source of (myo)fibroblasts is epithelial cells that undergo epithelial-mesenchymal transition (EMT), a process frequently mediated by TGF-beta. In this issue of the JCI, Kim et al. report that epithelial cell-specific deletion of alpha3 integrin prevents EMT in mice, thereby protecting against bleomycin-induced fibrosis (see the related article beginning on page 213). The authors propose a novel mechanism linking TGF-beta and beta-catenin signaling in EMT through integrin-dependent association of tyrosine-phosphorylated beta-catenin and pSmad2 and suggest targeted disruption of this interaction as a potential therapeutic approach.
authors.affiliation: Will Rogers Institute Pulmonary Research Center, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Southern California, Los Angeles, CA 90033, USA. zborok@usc.edu
authors.forename: Zea
authors.initials: Z
authors.lastname: Borok
mesh_terms: D000818:Animals; D000903:Antibiotics, Antineoplastic / Q000378:metabolism; D001761:Bleomycin / Q000378:metabolism; D002454:Cell Differentiation / Q000502:physiology*; D004847:Epithelial Cells / Q000502:physiology*; D005109:Extracellular Matrix / Q000378:metabolism; D006801:Humans; D039422:Integrin alpha3 / Q000235:genetics / Q000378:metabolism*; D008648:Mesoderm / Q000166:cytology / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction / Q000502:physiology; D051153:Wnt Proteins / Q000378:metabolism; D051176:beta Catenin / Q000378:metabolism
chemical_list: D000903:Antibiotics, Antineoplastic; D039422:Integrin alpha3; D051153:Wnt Proteins; D051176:beta Catenin; D001761:Bleomycin