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Prepublished online as a Blood First Edition Paper on November 21, 2002; DOI 10.1182/blood-2002-05-1363. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-05-1363v1 101/7/2646    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 Cho, M. J. Articles by Gartner, T. K. Search for Related Content PubMed PubMed Citation Articles by Cho, M. J. Articles by Gartner, T. K. 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. 2646-2651 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY The roles of IIb3-mediated outside-in signal transduction, thromboxane A2, and adenosine diphosphate in collagen-induced platelet aggregation Moon J. Cho, Junling Liu, Tamara I. Pestina, Shirley A. Steward, Dennis W. Thomas, Thomas M. Coffman, Demin Wang, Carl W. Jackson, and T. Kent Gartner From the Department of Microbiology and Molecular Cell Sciences, University of Memphis, Memphis, TN; the Division of Experimental Hematology, St Jude Children's Research Hospital, Memphis, TN; the Department of Medicine, Duke University and Durham Veterans Affairs Medical Centers, Durham, NC; and the Blood Research Institute, Blood Center of SE Wisconsin, Milwaukee. Collagen-induced activation of platelets in suspension leads to IIb3-mediated outside-in signaling, granule release, thromboxane A2 (TxA2) production, and aggregation. Although much is known about collagen-induced platelet signaling, the roles of TxA2 production, adenosine diphosphate (ADP) and dense-granule secretion, and IIb3-mediated outside-in signaling in this process are unclear. Here, we demonstrate that TxA2 and ADP are required for collagen-induced platelet activation in response to a low, but not a high, level of collagen and that IIb3-mediated outside-in signaling is required, at least in part, for this TxA2 production and ADP secretion. A high level of collagen can activate platelets deficient in PLC2, Gq, or TxA2 receptors, as well as platelets treated with a protein kinase C inhibitor, Ro31-8220. Thus, activation of IIb3 in response to a high level of collagen does not require these signaling proteins. Furthermore, a high level of collagen can cause weak TxA2 and ADP-independent aggregation, but maximal aggregation induced by a high level of collagen requires TxA2 or secretion. © 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: J. A. Coppinger, R. O'Connor, K. Wynne, M. Flanagan, M. Sullivan, P. B. Maguire, D. J. Fitzgerald, and G. Cagney Moderation of the platelet releasate response by aspirin Blood, June 1, 2007; 109(11): 4786 - 4792. [Abstract] [Full Text] [PDF] D. Yacoub, J.-F. Theoret, L. Villeneuve, H. Abou-Saleh, W. Mourad, B. G. Allen, and Y. Merhi Essential Role of Protein Kinase C{delta} in Platelet Signaling, {alpha}IIbbeta3 Activation, and Thromboxane A2 Release J. Biol. Chem., October 6, 2006; 281(40): 30024 - 30035. [Abstract] [Full Text] [PDF] N. O'Kennedy, L. Crosbie, M. van Lieshout, J. I Broom, D. J Webb, and A. 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