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Plasminogen activator inhibitor-1 secretion of endothelial cells increases
fibrinolytic resistance of an in vitro fibrin clot: evidence for a key role
of endothelial cells in thrombolytic resistance
S Handt, WG Jerome, L Tietze and RR Hantgan
Department of Pathology, Aachen University of Technology, Germany.
Time-dependent thrombolytic resistance is a critical problem in
thrombolytic therapy for acute myocardial infarction. Platelets have been
regarded as the main source of plasminogen activator inhibitor-1 (PAI-1)
found in occlusive platelet-rich clots. However, endothelial cells are also
known to influence the fibrinolytic capacity of blood vessels, but their
ability to actively mediate time-dependent thrombolytic resistance has not
been fully established. We will show that, in vitro, tumor necrosis
factor-alpha-stimulated endothelial cells secrete large amounts of PAI-1
over a period of hours, which then binds to fibrin and protects the clot
from tissue plasminogen activator- induced fibrinolysis. In vivo,
endothelial cells covering atherosclerotic plaques are influenced by
cytokines synthesized by plaque cells. Therefore, we propose that
continuous activation of endothelial cells in atherosclerotic blood
vessels, followed by elevated PAI-1 secretion and storage of active PAI-1
in the fibrin matrix, leads to clot stabilization. This scenario makes
endothelial cells a major factor in time-dependent thrombolytic resistance.
Volume 87,
Issue 10,
pp. 4204-4213,
05/15/1996
Copyright © 1996 by The American Society of Hematology
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