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Blood, Vol. 95 No. 2 (January 15), 2000:
pp. 577-580
Plasminogen activator inhibitor-1 and vitronectin promote
vascular thrombosis in mice
Daniel T. Eitzman,
Randal J. Westrick,
Elizabeth
G. Nabel, and
David Ginsburg
From the Cardiovascular Research Center and Division of Molecular
Medicine and Human Genetics, Department of Internal Medicine, and the
Howard Hughes Medical Institute, University of Michigan Medical Center,
Ann Arbor, MI.
Occlusive thrombosis depends on the net balance between platelets,
coagulation, and fibrinolytic factors. Epidemiologic information suggests that plasminogen activator inhibitor-1 (PAI-1), a central regulator of the fibrinolytic system, plays an important role in
determining the overall risk for clinically significant vascular thrombosis. Vitronectin (VN), an abundant plasma and matrix
glycoprotein, binds PAI-1 and stabilizes its active conformation. This
study assessed the role of PAI-1 and VN expression in the formation of
occlusive vascular thrombosis following arterial or venous injury. The
common carotid arteries of 17 wild-type (WT) mice and 8 mice deficient
in PAI-1 were injured photochemically while blood flow was continuously
monitored. WT mice developed occlusive thrombi at 52.0 ± 3.8 minutes
(mean ± SEM) following injury; mice deficient in PAI-1 developed
occlusive thrombosis at 127 ± 15 minutes
(P < .0001). Mice deficient in VN (n = 12)
developed vascular occlusion 77 ± 11 minutes after injury,
intermediate between the values observed for WT mice
(P < .03) and mice deficient in PAI-1 (P < .01). PAI-1 and VN also affected the time to occlusion
after injury to the jugular vein. Three WT mice developed
occlusive venous thrombosis an average of 39.7 ± 1 minutes following
the onset of injury, whereas the jugular veins of 4 mice deficient in
PAI-1 and 4 deficient in VN occluded 56.7 ± 5 and 58.7 ± 2 minutes,
respectively, following injury (P < .04 and
P < .01 compared to WT mice). These results suggest that
endogenous fibrinolysis and its regulation by PAI-1 and VN have
important roles in the development of occlusive vascular thrombosis
after vascular injury.
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