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Blood, 15 August 2004, Vol. 104, No. 4, pp. 1034-1041. Prepublished online as a Blood First Edition Paper on April 6, 2004; DOI 10.1182/blood-2003-12-4293. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-12-4293v1 104/4/1034    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 Wu, Y.-P. Articles by de Boer, H. C. Search for Related Content PubMed PubMed Citation Articles by Wu, Y.-P. Articles by de Boer, H. C. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Fibrin-incorporated vitronectin is involved in platelet adhesion and thrombus formation through homotypic interactions with platelet-associated vitronectin Ya-Ping Wu, Haiko J. Bloemendal, Emile E. Voest, Ton Logtenberg, Philip G. de Groot, Martijn F. B. G. Gebbink, and Hetty C. de Boer From the Departments of Haematology, Medical Oncology, and Immunology, University Medical Centre, Utrecht, the Netherlands; and Department of Nephrology, Leiden University Medical Centre, the Netherlands. When a blood clot is formed, vitronectin (VN) is incorporated. Here we studied the consequence of VN incorporation for platelet interactions under flow. Perfusion of whole blood over a fibrin network, formed from purified fibrinogen, resulted in approximately 20% surface coverage with blood platelets. Incorporation of purified multimeric VN into the fibrin network resulted in a 2-fold increase in surface coverage with platelets and in enhancement of platelet aggregate formation. A human monoclonal antibody (huMab VN18), directed against the multimeric form of VN, inhibited platelet adhesion to the combined fibrin/VN matrix to the level of adhesion on fibrin alone. This inhibition was also shown when whole blood was perfused over a plasma-derived clot. Surprisingly, the inhibitory action of the antibody was not directed toward VN incorporated into the fibrin network but toward VN released from the platelets. We conclude that VN-potentiated platelet-clot interaction requires VN in the clot and multimeric VN bound to the platelet surface. Our results provide evidence that homotypic VN interactions contribute to platelet adhesion and aggregation to a blood clot. This report demonstrates for the first time that self-assembly of VN may provide a physiologically relevant contribution to platelet aggregation on a blood clot. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Reheman, H. Yang, G. Zhu, W. Jin, F. He, C. M. Spring, X. Bai, P. L. Gross, J. Freedman, and H. Ni Plasma fibronectin depletion enhances platelet aggregation and thrombus formation in mice lacking fibrinogen and von Willebrand factor Blood, February 19, 2009; 113(8): 1809 - 1817. [Abstract] [Full Text] [PDF] C.T. Whitlow, C.P. Geer, C.W.T. Mattern, B.J. Mussat-Whitlow, S.K. Yazdani, J.L. Berry, J.H. Lalli, R.O. Claus, V.R. Challa, and P.P. Morris Endovascular Histologic Effects of Ultrathin Gold- or Vitronectin-Coated Platinum Aneurysm Coils in a Rodent Arterial Occlusion Model: A Preliminary Investigation AJNR Am. J. Neuroradiol., January 1, 2009; 30(1): 85 - 90. [Abstract] [Full Text] [PDF]

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