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This Article Full Text Full Text (PDF) 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 André, P. Articles by Wagner, D. D. Search for Related Content PubMed PubMed Citation Articles by André, P. Articles by Wagner, D. D. Related Collections Plenary Papers Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 November 2000, Vol. 96, No. 10, pp. 3322-3328 PLENARY PAPER Platelets adhere to and translocate on von Willebrand factor presented by endothelium in stimulated veins Patrick André, Cécile V. Denis, Jerry Ware, Simin Saffaripour, Richard O. Hynes, Zaverio M. Ruggeri, and Denisa D. Wagner From the Center for Blood Research and the Department of Pathology, Harvard Medical School, Boston, MA; the Roon Research Center for Arteriosclerosis and Thrombosis, The Scripps Research Institute, La Jolla, CA; and the Howard Hughes Medical Institute, Center for Cancer Research, Massachusetts Institute of Technology, Cambridge, MA. With the use of intravital microscopy, a new type of platelet-endothelial interaction in mouse mesenteric venules at low shear (80-100 seconds1) is described. Stimulation of these vessels with calcium ionophore A23187, a known secretagogue of Weibel-Palade bodies, induced immediate platelet adhesion (within 15 seconds) and translocation without the formation of aggregates. This stop-and-go process reached a maximum in approximately 1 minute, when approximately 25 000 platelets adhered/mm2·s, and then adhesion progressively decreased. This adhesion process was dependent on von Willebrand factor (vWF) and independent of P-selectin. Immunohistologic analysis showed that the venules were not denuded with A23187 treatment, suggesting that platelets adhered to vWF secreted on the luminal face of the endothelial cells. Histamine treatment induced a similar adhesion phenomenon. Platelet adhesion was not abolished in 3-deficient mice or when the platelets were treated with inhibitory antibodies to PECAM-1 or PSGL-1, indicating that these molecules are not required for platelet-endothelium interaction at low shear. The adhesion was mediated by platelet glycoprotein Ib (GPIb) because the adhesion of murine platelets expressing exclusively the human GPIb could be prevented by a pretreatment with mocarhagin, a snake venom protease that cleaves human GPIb. The results indicate that vWF released from Weibel-Palade bodies can dramatically increase the concentration of platelets along the vessel wall through an interaction with GPIb. It is proposed that this process may rapidly recruit platelets to sites of injury or inflammation in veins. © 2000 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: D. F. Cutler Fishing for platelets Blood, February 12, 2009; 113(7): 1397 - 1398. [Full Text] [PDF] J. Huang, R. Roth, J. E. Heuser, and J. E. Sadler Integrin {alpha}v{beta}3 on human endothelial cells binds von Willebrand factor strings under fluid shear stress Blood, February 12, 2009; 113(7): 1589 - 1597. [Abstract] [Full Text] [PDF] D. D. Wagner and P. S. Frenette The vessel wall and its interactions Blood, June 1, 2008; 111(11): 5271 - 5281. [Abstract] [Full Text] [PDF] M. Erent, A. Meli, N. Moisoi, V. Babich, M. J. 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