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J Clin Invest. 2009 Jan;119(1):7-10. doi: 10.1172/JCI38084.

Role for alpha3 integrin in EMT and pulmonary fibrosis.

Author information

1
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

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.

PMID:
19104143
PMCID:
PMC2613449
DOI:
10.1172/JCI38084
[Indexed for MEDLINE]
Free PMC Article

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