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Published ahead of print on August 28, 2003, doi:10.1164/rccm.200212-1514OC
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American Journal of Respiratory and Critical Care Medicine Vol 168. pp. 1156-1161, (2003)
© 2003 American Thoracic Society

Defect of Hepatocyte Growth Factor Secretion by Fibroblasts in Idiopathic Pulmonary Fibrosis

Sylvain Marchand-Adam, Joëlle Marchal, Murielle Cohen, Paul Soler, Bénédicte Gerard, Yves Castier, Guy Lesèche, Dominique Valeyre, Hervé Mal, Michel Aubier, Monique Dehoux and Bruno Crestani

INSERM unit 408, Faculté Xavier Bichat; and Service de Pneumologie, Laboratoire de Biochimie A, and Laboratoire de Biochimie Hormonale et Génétique, Hôpital Bichat, Assistance Publique-Hôpitaux de Paris, Paris; Service de Chirurgie Thoracique et Vasculaire and Service de Pneumologie, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy; and Service de Pneumologie, Hôpital Avicenne, Bobigny, France

Correspondence and requests for reprints should be addressed to Bruno Crestani, M.D., Service de Pneumologie, Hôpital Bichat, 16 rue Henri Huchard, 75877 Paris Cedex 18, France. E-mail: bruno.crestani{at}bch.ap-hop-paris.fr

Hepatocyte growth factor (HGF) is a growth factor that protects alveolar epithelial cells from pulmonary fibrosis in various animal models. We compared in vitro HGF production by human lung fibroblasts from patients with idiopathic pulmonary fibrosis (IPF, n = 8) and from control subjects (n = 6). Basal HGF secretion by IPF fibroblasts was decreased by 50% when compared with control fibroblasts (p < 0.05). HGF was secreted mainly in the cleaved mature form, both in IPF and control fibroblasts. HGF messenger RNA levels were reduced in IPF fibroblasts. Prostaglandin (PG) E2 secretion by IPF fibroblasts was low when compared with control subjects (p < 0.05). After the addition of PGE2 (10-6 M) or dibutyryl cyclic AMP (10-3 M), HGF secretion by IPF fibroblasts reached the level of control subjects. Inhibition of PGE2 synthesis with indomethacin reduced HGF secretion by control fibroblasts but had no effect on IPF fibroblasts. HGF secretion by control fibroblasts was also slightly inhibited by transforming growth factor (TGF)-ß1 and stimulated by anti–TGF-ß antibody, whereas both agents had no effect on IPF fibroblasts. Our results demonstrate a defect in HGF production by IPF fibroblasts that seems secondary to a defect in PGE2 secretion.

Key Words: indomethacin • pulmonary alveoli • transforming growth factor ß • usual interstitial pneumonia




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