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Research Article Free access | 10.1172/JCI116144

Fibrinogen degradation product fragment D induces endothelial cell detachment by activation of cell-mediated fibrinolysis.

M Ge, G Tang, T J Ryan, and A B Malik

Department of Physiology and Cell Biology, Albany Medical College of Union University, New York 12208.

Find articles by Ge, M. in: PubMed | Google Scholar

Department of Physiology and Cell Biology, Albany Medical College of Union University, New York 12208.

Find articles by Tang, G. in: PubMed | Google Scholar

Department of Physiology and Cell Biology, Albany Medical College of Union University, New York 12208.

Find articles by Ryan, T. in: PubMed | Google Scholar

Department of Physiology and Cell Biology, Albany Medical College of Union University, New York 12208.

Find articles by Malik, A. in: PubMed | Google Scholar

Published December 1, 1992 - More info

Published in Volume 90, Issue 6 on December 1, 1992
J Clin Invest. 1992;90(6):2508–2516. https://doi.org/10.1172/JCI116144.
© 1992 The American Society for Clinical Investigation
Published December 1, 1992 - Version history
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Abstract

We studied the effects of fibrinogen degradation product (FDP) fragment D on endothelial monolayer integrity and the mechanisms of fragment D-induced endothelial cell detachment from the substratum. Incubation of bovine pulmonary artery endothelial cells (BPAEC) with fragment D caused concentration- and time-dependent cell detachment from the substratum. The optimal response occurred at fragment D concentrations of 2 microM and required an incubation time of 24 h. BPAEC challenged with fragment D increased the concentration and activity of urokinase-type plasminogen activator (uPA) in the conditioned medium within 2 to 4 h of incubation. Fragment D also induced the release of tissue-type plasminogen activator, but to a lesser extent than uPA. Fragment D concurrently increased plasminogen activator (PA) activity in a concentration-dependent manner. Increased PA activity was followed by augmentation of cell-associated plasmin activity and subsequent increase in the degradation of 125I-fibrinogen and 125I-vitronectin precoated in the subendothelial matrix. Pretreatment of BPAEC with anti-uPA antibody, and inhibitors of uPA (dansyl-GGACK) and plasmin (aprotinin) prevented approximately 60% of the fragment D-induced endothelial cell detachment. We conclude that FDP fragment D increases secretion of endothelial PAs and enhances the generation of plasmin, thereby contributing to proteolysis of extracellular matrix and endothelial cell detachment. Fragment D may be a critical mediator linking activation of fibrinolysis to vascular endothelial injury in inflammatory disorders.

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