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Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:877-878
doi: 10.1161/01.ATV.0000161049.53535.5d
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:877.)
© 2005 American Heart Association, Inc.


Editorials

P-Selectin and Blood Coagulation

It’s Not Only About Inflammation Any More

Bruce Furie

From the Harvard Medical School, Boston, Mass.

Correspondence to Bruce Furie, Harvard Medical School, 330 Brookline Ave, Boston, MA 02215. E-mail bfurie@bidmc.harvard.edu


An extract of the first 250 words of the full text is provided, because this article has no abstract.
 

Although P-selectin had already been established as a vascular adhesion molecule critical in the inflammatory response, in 1992 Palabrica et al were the first to demonstrate that P-selectin also played a significant role in blood coagulation and thrombosis.1 In these experiments using an arteriovenous shunt model of thrombosis in a baboon, anti–P-selectin antibodies were shown to block fibrin formation in the developing thrombus forming in a thrombogenic Dacron shunt. Shortly thereafter, P-selectin was not only shown to upregulate tissue factor generation in monocytes,2 but also to initiate signaling pathways in leukocytes and activate the elaboration of cytokines in a mechanism that involved P-selectin interaction with its receptor, PSGL-1.3,4 A number of more recent reports have secured a role for P-selectin in hemostasis and thrombosis, including the demonstration that overexpression of P-selectin can induce a procoagulant state,5 that circulating microparticles bearing PSGL-1, the counterreceptor for P-selectin, deliver tissue factor to the growing platelet thrombus via a mechanism dependent on P-selectin and PSGL-1,6 and that procoagulant microparticles can partially correct the hemostatic defect in hemophilic mice.7 The role of P-selectin and PSGL-1 along with microparticles has recently been reviewed.8,9 The current report by del Conde et al in this issue of Arteriosclerosis, Thrombosis, and Vascular Biology10 adds yet another page to the growing list of mechanisms by which P-selectin can contribute to procoagulant activity.

See page 1065

The current study demonstrates that the interaction of P-selectin with PSGL-1 on monocytes or monocyte-like cells is associated with the exposure of phosphatidylserine on the . . . [Full Text of this Article]


Related Article:

Effect of P-Selectin on Phosphatidylserine Exposure and Surface-Dependent Thrombin Generation on Monocytes
Ian del Conde, Faisal Nabi, Raúl Tonda, Perumal Thiagarajan, José A. López, and Neal S. Kleiman
Arterioscler Thromb Vasc Biol 2005 25: 1065-1070. [Abstract] [Full Text] [PDF]