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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.
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Submitted October 27, 2004
Accepted February 11, 2005
Young thrombocytes initiate the formation of arterial thrombus in zebrafish
Bijoy Thattliyath, Matthew Cykowski, and Pudur Jagadeeswaran*
Department of Cellular and Structural Biology, The University of Texas Health Science Center, San Antonio, TX, USA
* Corresponding author; email: Jagadeeswar{at}UTHSCSA.edu.
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 physiological 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 two 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 thrombocytes 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 sub-endothelial 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, the above mechanism may be conserved in mammals and may open new avenues for prevention of arterial thrombosis.
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