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ENA-78 is an important angiogenic factor in idiopathic pulmonary fibrosis

M P Keane1, J A Belperio, M D Burdick

  • 1Division of Pulmonary and Critical Care Medicine, Department of Medicine, UCLA School of Medicine, Los Angeles, California 90095-1922, USA. mpkeane@mednet.ucla.edu

American Journal of Respiratory and Critical Care Medicine
|December 26, 2001
PubMed

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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