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Intimal Tissue Factor Activity Is Released from the Arterial Wall after Injury

Journal: Thrombosis and Haemostasis
ISSN: 0340-6245
Issue: 2000: 83/4 (Apr) pp.520-636
Pages: 622-636

Intimal Tissue Factor Activity Is Released from the Arterial Wall after Injury

Peter L. A. Giesen (1), (3), * , Billie S. Fyfe (4), * * , John T. Fallon (2), (3), (4) , Merce Roque (2), (3) , Milton Mendlowitz (3) , Maria Rossikhina (2), (3) , Arabinda Guha (1), (3) , Juan J. Badimon (2), (3) , Yale Nemerson (1), (3) , Mark B. Tau
From the (1) Division of Thrombosis Research and (2) The Zena and Michael A. Wiener Cardiovascular Institute, (3) Department of Medicine, and (4) Department of Pathology, The Mount Sinai School of Medicine, New York, NY, USA

Summary

Tissue factor (TF), the initiator of coagulation, has been implicated as a critical mediator of arterial thrombosis. Previous studies have demonstrated that TF is rapidly induced in the normal rodent arterial wall by balloon injury, but is not associated with fibrin deposition. A second injury, however, performed 10-14 days after the first, is followed by small platelet-fibrin microthrombi. This study was undertaken to better localize active TF in balloon-injured rat arteries and to explore possible mechanisms underlying the apparent discrepancy between injury-induced TF expression and the lack of large plateletfibrin thrombi. By immunohistochemistry, TF antigen was first detected in the media 24 h after injury to rat aortas, and subsequently accumulated in the neointima. Using an ex vivo flow chamber, no TF activity (Factor Xa generation) was found on the luminal surface of normal or injured aortas. Wiping the luminal surface with a cotton swab exposed TF activity in all vessels; levels were increased ≈3-fold in arteries containing a neointima. The exposed TF activity was rapidly washed into the perfusate, rendering the luminal surface inactive. The loss of luminal TF into the circulation may attenuate thrombosis at sites of arterial injury.