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Cyclooxygenase-2 Overexpression, Using an Integrin-Targeted Gene Delivery System (the LID Vector), Inhibits Fibroblast Proliferation In Vitro and Leads to Increased Prostaglandin E2 in the Lung*

Gisli Jenkins, MD; Stephen L. Hart, PhD; Rebecca J. Hodges, BSc; Qin-Hai Meng, MD, PhD; Christine Kinnon, PhD; Geoffrey J. Laurent, PhD; Robin J. McAnulty, PhD
Author and Funding Information

*From the Centre for Respiratory Research, Rayne Institute, and Institute of Child Health, University College London, London UK.

Correspondence to: Gisli Jenkins, MD, Centre for Respiratory Research, Royal Free and University College Medical School, Rayne Institute, 5 University St, London WC1E 6JJ; e-mail: gjloffice@ucl.ac.uk



Chest. 2002;121(3_suppl):102S-104S. doi:10.1378/chest.121.3_suppl.102S
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Pulmonary fibrosis is a progressive and fatal disease for which there is no effective treatment. It is characterized by increased matrix deposition following an apparent, or subclinical, lung injury. The fibrogenic process often is preceded by inflammation, which is best characterized in animal models. In this process, prostaglandin E2 (PGE2) is the major prostanoid secreted by both fibroblasts and stimulated inflammatory cells. Cyclooxygenase (COX) is the rate-limiting enzyme in prostanoid biosynthesis. There are two isoforms. COX-1 is the constitutive isoform, which is thought to be responsible for housekeeping functions, and COX-2 is the inducible isoform, which is known to be up-regulated early in acute inflammatory conditions. However, little attention has been paid to understanding the mechanisms by which proinflammatory and profibrotic responses are inhibited during injury and terminated following injury, thus preventing the development of fibrosis.

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