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Prepublished online as a Blood First Edition Paper on December 12, 2002; DOI 10.1182/blood-2002-07-2209. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-07-2209v1 101/7/2661    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Burger, P. C. Articles by Wagner, D. D. Search for Related Content PubMed PubMed Citation Articles by Burger, P. C. Articles by Wagner, D. D. Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 April 2003, Vol. 101, No. 7, pp. 2661-2666 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Platelet P-selectin facilitates atherosclerotic lesion development Peter C. Burger and Denisa D. Wagner From the Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, MA. P-selectin is an adhesion molecule expressed on activated platelets and endothelium. It is known to play an important role in atherosclerosis. P-selectin also circulates in plasma in a soluble form (sP-selectin), which induces procoagulant microparticle formation. We investigated the role of platelet versus endothelial P-selectin in generating sP-selectin and in the formation of atherosclerotic lesions in the apolipoprotein E (apoE)-deficient mouse model. For this we transplanted apoE/P-selectin/ and apoE/P-selectin+/+ lethally irradiated mice with bone marrow of either genotype. Seven months after transplantation, we determined from the chimeric animals that the majority of circulating sP-selectin was of endothelial origin. Thus, in atherosclerosis, the procoagulant sP-selectin reflects endothelial rather than platelet activation. We found that endothelial P-selectin was crucial for the promotion of atherosclerotic lesion growth because in its absence only relatively small lesions developed. However, platelet P-selectin also contributed to the lesion development because lesions in wild-type recipients receiving transplants with wild-type platelets were 30% larger than those receiving P-selectin-deficient platelets (P < .008) and were more frequently calcified (80% versus 44%). In comparison with P-selectin wild-type animals, absence of either endothelial or platelet P-selectin inhibited migration of smooth muscle cells into the lesion. Thus, in addition to endothelium, platelets and their P-selectin also actively promote advanced atherosclerotic lesion development. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: V. S. Dole, J. Matuskova, E. Vasile, A. Yesilaltay, W. Bergmeier, M. Bernimoulin, D. D. Wagner, and M. Krieger Thrombocytopenia and Platelet Abnormalities in High-Density Lipoprotein Receptor-Deficient Mice Arterioscler. Thromb. Vasc. Biol., June 1, 2008; 28(6): 1111 - 1116. [Abstract] [Full Text] [PDF] T. Goerge, B. Ho-Tin-Noe, C. Carbo, C. Benarafa, E. Remold-O'Donnell, B.-Q. Zhao, S. M. Cifuni, and D. D. Wagner Inflammation induces hemorrhage in thrombocytopenia Blood, May 15, 2008; 111(10): 4958 - 4964. 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