Thromb Haemost 1995; 74(06): 1573-1577
DOI: 10.1055/s-0038-1649984
Original Articles
Vessel Wall
Schattauer GmbH Stuttgart

Procoagulant Albumin Increases Vascular Endothelial Cell Prostacyclin Secretion

David B Gubler
1   The Department of Medicine, University of Utah, Health Sciences Center, UT, USA
,
Chad R Ahlstrom
1   The Department of Medicine, University of Utah, Health Sciences Center, UT, USA
,
Lihua Liu
1   The Department of Medicine, University of Utah, Health Sciences Center, UT, USA
,
Jin-Feng Zhou
1   The Department of Medicine, University of Utah, Health Sciences Center, UT, USA
,
Charles J Parker
1   The Department of Medicine, University of Utah, Health Sciences Center, UT, USA
3   The Department of Veterans Affairs Medical Center, Salt Lake City, UT, USA
,
George M Rodgers
1   The Department of Medicine, University of Utah, Health Sciences Center, UT, USA
2   The Department of Pathology, University of Utah, Health Sciences Center, UT, USA
3   The Department of Veterans Affairs Medical Center, Salt Lake City, UT, USA
› Author Affiliations
Further Information

Publication History

Received 20 April 1995

Accepted after resubmission16 August 1995

Publication Date:
10 July 2018 (online)

Summary

Vascular endothelium regulates multiple aspects of platelet function through secretion of a variety of substances, including von Willebrand factor, nitric oxide, and prostacyclin (PGI2). The objective of this study was to determine whether procoagulant albumin (P-AI), a modified form of albumin present in normal human plasma could modulate endothelial cell secretion of these substances. P-AI did not affect constitutive secretion of von Willebrand factor or nitric oxide, but did increase PGI2 secretion in a time- and concentration-dependent manner. Pretreatment of endothelial cells with aspirin, or use of suramin, a broad- specificity inhibitor, prevented the response to P-AI. Prostaglandin H synthase-2 contributed to the P-AI-induced PGI2 secretion. These results indicate that in addition to inducing tissue factor activity and reducing protein C activation and fibrinolysis, P-AI also modulates vascular endothelial cell PGI2 secretion, and potentially, platelet function.

 
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