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Fibrin Fragment Response Elements in the Plasminogen Activator Inhibitor Gene*

M.A. Olman, MD; J.S. Hagood, MD; W.L. Simmons; K.E. White
Author and Funding Information

*From the Divisions of Pulmonary and Critical Care Medicine and Pediatric Pulmonology, University of Alabama at Birmingham, Birmingham, AL.

Correspondence to: M.A. Olman, MD, Division of Pulmonary and Critical Care Medicine, University of Alabama at Birmingham, 1900 University Blvd, THT 215, Birmingham, AL 35294-0006; e-mail: olman@pulm.dom.uab.edu



Chest. 1999;116(suppl_1):118S-119S. doi:10.1378/chest.116.suppl_1.118S
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Extract

The fibrinolytic protease inhibitor plasminogen activator inhibitor type I (PAI-1) dramatically affects the outcome of lung inflammation and fibrosis in mice injured with either bleomycin or hyperoxia. Furthermore, during human and/or experimental lung injury, fibrin deposition colocalizes with high PAI-1, expressing alveolar mesenchymal cells in the remodeling alveolar matrix. As we have recently shown that PAI-1 is transcriptionally upregulated in lung fibroblasts by the major plasmin proteolytic fragment of fibrin (D-dimer), we undertook this study to determine the cis-acting elements and trans-acting factors that are responsible for fibrin D-dimer’s action on PAI-1 transcription.


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