Am. J. Respir. Crit. Care Med., Volume 164, Number 12, December 2001, 2239-2242

ENA-78 Is an Important Angiogenic Factor in Idiopathic Pulmonary Fibrosis

MICHAEL P. KEANE, JOHN A. BELPERIO, MARIE D. BURDICK, JOSEPH P. LYNCH III, MICHAEL C. FISHBEIN, and ROBERT M. STRIETER

Division of Pulmonary and Critical Care Medicine, Department of Medicine, and Department of Pathology, UCLA School of Medicine, Los Angeles, California; and Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan

Idiopathic pulmonary fibrosis (IPF) is a chronic and often fatal disorder. Fibroplasia and deposition of extracellular matrix are dependent, in part, on angiogenesis and vascular remodeling. We obtained open lung biopsies from patients undergoing thoracic surgery for reasons other than interstitial lung disease (control) (n = 78) and from patients with IPF (n = 91). We found that levels of epithelial neutrophil-activating peptide 78 (ENA-78) were greater from tissue specimens of IPF patients, as compared with control subjects. When ENA-78 was depleted from IPF tissue specimens, tissue-derived angiogenic activity was markedly reduced. Immunolocalization of ENA-78 demonstrated that hyperplastic Type II pneumocytes and macrophages were the predominant cellular sources of ENA-78. These findings support the notion that ENA-78 may be an important additional factor that regulates angiogenic activity in IPF.

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