Prostaglandin E2 inhibits fibroblast chemotaxis

1  Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, Omaha 68198-5125; 3  Veterans Affairs Medical Center, Omaha, Nebraska 68105; 2  University of Milan, Milan 20122, Italy; 4  First Department of Pathology, Nippon Medical School, Tokyo 113-0022; and 5  Third Depar...

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Published in:American journal of physiology. Lung cellular and molecular physiology 2001-11, Vol.281 (5), p.1257
Main Authors: Kohyama, Tadashi, Ertl, Ronald F, Valenti, Vincenzo, Spurzem, John, Kawamoto, Masashi, Nakamura, Yoichi, Veys, Tom, Allegra, Luigi, Romberger, Debra, Rennard, Stephen I
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Language:English
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Summary:1  Pulmonary and Critical Care Medicine Section, University of Nebraska Medical Center, Omaha 68198-5125; 3  Veterans Affairs Medical Center, Omaha, Nebraska 68105; 2  University of Milan, Milan 20122, Italy; 4  First Department of Pathology, Nippon Medical School, Tokyo 113-0022; and 5  Third Department of Internal Medicine, University of Tokushima, Tokushima 770-8503, Japan Fibroblasts are the major source of extracellular connective tissue matrix, and the recruitment, accumulation, and stimulation of these cells are thought to play important roles in both normal healing and the development of fibrosis. Prostaglandin E 2 (PGE 2 ) can inhibit this process by blocking fibroblast proliferation and collagen production. The aim of this study was to investigate the inhibitory effect of PGE 2 on human plasma fibronectin (hFN)- and bovine bronchial epithelial cell-conditioned medium (BBEC-CM)-induced chemotaxis of human fetal lung fibroblasts (HFL1). Using the Boyden blind well chamber technique, PGE 2 (10 7 M) inhibited chemotaxis to hFN 40.8 ± 5.3% ( P  
ISSN:1040-0605
1522-1504
DOI:10.1152/ajplung.2001.281.5.l1257