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Blood, 1 July 2005, Vol. 106, No. 1, pp. 118-124. Prepublished online as a Blood First Edition Paper on March 15, 2005; DOI 10.1182/blood-2004-10-4118. This Article Full Text Full Text (PDF) Supplemental Movie All Versions of this Article: 2004-10-4118v1 106/1/118    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 Thattaliyath, B. Articles by Jagadeeswaran, P. Search for Related Content PubMed PubMed Citation Articles by Thattaliyath, B. Articles by Jagadeeswaran, P. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Signal Transduction Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Young thrombocytes initiate the formation of arterial thrombi in zebrafish Bijoy Thattaliyath, Matthew Cykowski, and Pudur Jagadeeswaran From the Department of Cellular and Structural Biology, The University of Texas Health Science Center, San Antonio TX. The zebrafish system is an excellent vertebrate genetic model to study hemostasis and thrombosis because saturation mutagenesis screens can identify novel genes that play a role in this vital physiologic pathway. To study hemostatic mutations, it is important to understand the physiology of zebrafish hemostasis and thrombosis. Previously, we identified zebrafish thrombocytes and have shown that they participate in arterial thrombus formation. Here, we recognized 2 populations of thrombocytes distinguishable by DiI-C18 (DiI) staining. DiI+ thrombocytes have a high density of adhesive receptors and are functionally more active than DiI– thrombocytes. We classified DiI+ thrombocytes as young and DiI– thrombocytes as mature thrombocytes. We found young and mature thrombocytes each formed independent clusters and that young thrombocytes clustered first. We have also shown that young thrombocytes initiate arterial thrombus formation. We propose that due to the increased adhesive receptor density on young thrombocytes, they adhere first to the subendothelial matrix, get activated rapidly, release agonists, and recruit more young thrombocytes, which further release more agonists. This increase in agonists activates the less active mature thrombocytes, drawing them to the growing thrombus. Since arterial thrombus formation is a fundamental hemostatic event, this mechanism may be conserved in mammals and may open new avenues for prevention of arterial thrombosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: The sticky matter of young versus old platelets Peter W. Marks Blood 2005 106: 7. [Full Text] [PDF] This article has been cited by other articles: D. Carradice and G. J. Lieschke Zebrafish in hematology: sushi or science? Blood, April 1, 2008; 111(7): 3331 - 3342. [Abstract] [Full Text] [PDF] R. K. Andrews, D. Karunakaran, E. E. Gardiner, and M. C. Berndt Platelet Receptor Proteolysis: A Mechanism for Downregulating Platelet Reactivity Arterioscler. Thromb. Vasc. Biol., July 1, 2007; 27(7): 1511 - 1520. [Abstract] [Full Text] [PDF] U. J.H. Sachs and B. Nieswandt In Vivo Thrombus Formation in Murine Models Circ. Res., April 13, 2007; 100(7): 979 - 991. [Abstract] [Full Text] [PDF] P. Jagadeeswaran A green light for the thrombopoietic program Blood, December 1, 2005; 106(12): 3684 - 3684. [Full Text] [PDF]

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