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Platelets stimulate endothelial cells to synthesize type 1 plasminogen
activator inhibitor. Evaluation of the role of transforming growth factor
beta
SR Slivka and DJ Loskutoff
Committee on Vascular Biology, Research Institute of Scripps Clinic, La
Jolla, CA 92037.
A model system consisting of thrombin-stimulated bovine platelet releasates
(PRthr) and bovine aortic endothelial cells (BAEs) was developed to
determine if the interaction between platelets and endothelial cells
regulates fibrinolysis. Zymographic analysis indicated that PRthr treatment
of BAEs decreases urokinase and increases type 1 plasminogen activator
inhibitor (PAI-1) activity. Although PRthr did not affect the overall rate
of BAE protein synthesis, it increased PAI-1 biosynthesis within 6 hours.
This increase was complete by 12 hours, with maximum stimulation at 10 to
15 micrograms/mL PRthr (1 microgram approximately 10(7) platelets).
Neutralizing antibodies to transforming growth factor beta (TGF beta)
reduced this effect by 75%. Treatments that activate latent TGF beta (eg,
acidification or plasmin) increased this effect approximately fivefold,
suggesting that TGF beta in PRthr exists in both a latent (approximately
80%) and an active (approximately 20%) form. In contrast to PRthr,
adenosine diphosphate-prepared platelet releasates did not increase PAI-1
synthesis before acidification, indicating that they contain only the
latent form of TGF beta. These results suggest that platelets can modulate
the fibrinolytic system of the endothelium through the release of TGF beta,
and that the mechanism by which the platelets are activated can influence
the relative amount of active TGF beta.
Volume 77,
Issue 5,
pp. 1013-1019,
03/01/1991
Copyright © 1991 by The American Society of Hematology
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