Published ahead of print on December 20, 2007, doi:10.1164/rccm.200708-1291OC
© 2008 American Thoracic Society doi: 10.1164/rccm.200708-1291OC
An Essential Role for Fibronectin Extra Type III Domain A in Pulmonary Fibrosis1 International Centre for Genetic Engineering and Biotechnology, Trieste, Italy; 2 Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, Michigan; and 3 Lung Biology Center, University of California at San Francisco, San Francisco, California Correspondence and requests for reprints should be addressed to Eric S. White, M.D., Division of Pulmonary and Critical Care Medicine, University of Michigan Medical School, 6301 MSRB III/0642, 1150 W. Medical Center Drive, Ann Arbor, MI 48109-0642. E-mail: docew{at}umich.edu Rationale: Tissue fibrosis is considered a dysregulated wound-healing response. Fibronectin containing extra type III domain A (EDA) is implicated in the regulation of wound healing. EDA-containing fibronectin is deposited during wound repair, and its presence precedes that of collagen. Objectives: To investigate the role of EDA-containing fibronectin in lung fibrogenesis.
Methods: Primary lung fibroblasts from patients with idiopathic pulmonary fibrosis or from patients undergoing resection for lung cancer were assessed for EDA-containing fibronectin and
Measurements and Main Results: Idiopathic pulmonary fibrosis lung fibroblasts produced markedly more EDA-containing fibronectin and Conclusions: The data show that EDA-containing fibronectin is essential for the fibrotic resolution of lung injury through TGF-β activation and responsiveness, and suggest that EDA-containing fibronectin plays a critical role in tissue fibrogenesis.
Key Words: fibrosis fibronectin TGF-β myofibroblast
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