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Blood, 15 June 2007, Vol. 109, No. 12, pp. 5087-5095. Prepublished online as a Blood First Edition Paper on February 20, 2007; DOI 10.1182/blood-2006-12-027698. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-12-027698v1 109/12/5087    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 Jackson, S. P. Search for Related Content PubMed PubMed Citation Articles by Jackson, S. P. Related Collections Cell Adhesion and Motility Cytoskeleton Signal Transduction Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  REVIEW ARTICLE The growing complexity of platelet aggregation Shaun P. Jackson Australian Centre for Blood Diseases, Monash University, Melbourne, Australia Platelet aggregation, the process by which platelets adhere to each other at sites of vascular injury, has long been recognized as critical for hemostatic plug formation and thrombosis. Until relatively recently, platelet aggregation was considered a straightforward process involving the noncovalent bridging of integrin IIbß3 receptors on the platelet surface by the dimeric adhesive protein fibrinogen. However, with recent technical advances enabling real-time analysis of platelet aggregation in vivo, it has become apparent that this process is much more complex and dynamic than previously anticipated. Over the last decade, it has become clear that platelet aggregation represents a multistep adhesion process involving distinct receptors and adhesive ligands, with the contribution of individual receptor-ligand interactions to the aggregation process dependent on the prevailing blood flow conditions. It now appears that at least 3 distinct mechanisms can initiate platelet aggregation, with each of these mechanisms operating over a specific shear range in vivo. The identification of shear-dependent mechanisms of platelet aggregation has raised the possibility that vascular-bed–specific inhibitors of platelet aggregation may be developed in the future that are safer and more effective than existing antiplatelet agents. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. T. Nurden Thrombus stability on the vessel wall Blood, July 1, 2008; 112(1): 4 - 5. [Full Text] [PDF] A. Ono, E. Westein, S. Hsiao, W. S. Nesbitt, J. R. Hamilton, S. M. Schoenwaelder, and S. P. Jackson Identification of a fibrin-independent platelet contractile mechanism regulating primary hemostasis and thrombus growth Blood, July 1, 2008; 112(1): 90 - 99. [Abstract] [Full Text] [PDF] N. Watanabe, L. Bodin, M. Pandey, M. Krause, S. Coughlin, V. A. Boussiotis, M. H. Ginsberg, and S. J. Shattil Mechanisms and consequences of agonist-induced talin recruitment to platelet integrin {alpha}IIb{beta}3 J. Cell Biol., June 25, 2008; 181(7): 1211 - 1222. [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. A. Berny, T. C. White, E. I. Tucker, L. A. Bush-Pelc, E. Di Cera, A. Gruber, and O. J.T. McCarty Thrombin Mutant W215A/E217A Acts as a Platelet GPIb Antagonist Arterioscler. Thromb. Vasc. Biol., February 1, 2008; 28(2): 329 - 334. [Abstract] [Full Text] [PDF]

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