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Blood, 16 July 2009, Vol. 114, No. 3, pp. 663-666. Prepublished online as a Blood First Edition Paper on April 22, 2009; DOI 10.1182/blood-2009-01-200345. This Article Full Text Full Text (PDF) Supplemental Methods and Figures All Versions of this Article: blood-2009-01-200345v1 114/3/663    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 Google Scholar Articles by Schoenwaelder, S. M. Articles by Jackson, S. P. PubMed PubMed Citation Articles by Schoenwaelder, S. M. Articles by Jackson, S. P. Related Collections Platelets and Thrombopoiesis Thrombosis and Hemostasis Brief Reports Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  PLATELETS AND THROMBOPOIESIS Brief report Two distinct pathways regulate platelet phosphatidylserine exposure and procoagulant function Simone M. Schoenwaelder1,*, Yuping Yuan1,*, Emma C. Josefsson2, Michael J. White2, Yu Yao1, Kylie D. Mason3, Lorraine A. O'Reilly3, Katya J. Henley2, Akiko Ono1, Sarah Hsiao1, Abbey Willcox1, Andrew W. Roberts4, David C. S. Huang3, Hatem H. Salem1, Benjamin T. Kile2,, and Shaun P. Jackson1, 1 Australian Centre for Blood Diseases, Monash University, Melbourne; Divisions of 2 Molecular Medicine, 3 Molecular Genetics of Cancer, and 4 Cancer and Hematology, The Walter and Eliza Hall Institute (WEHI) of Medical Research, Parkville, Australia Procoagulant platelets exhibit hallmark features of apoptotic cells, including membrane blebbing, microvesiculation, and phosphatidylserine (PS) exposure. Although platelets possess many well-known apoptotic regulators, their role in regulating the procoagulant function of platelets is unclear. To clarify this, we investigated the consequence of removing the essential mediators of apoptosis, Bak and Bax, or directly inducing apoptosis with the BH3 mimetic compound ABT-737. Treatment of platelets with ABT-737 triggered PS exposure and a marked increase in thrombin generation in vitro. This increase in procoagulant function was Bak/Bax- and caspase-dependent, but it was unaffected by inhibitors of platelet activation or by chelating extracellular calcium. In contrast, agonist-induced platelet procoagulant function was unchanged in Bak–/–Bax–/– or caspase inhibitor–treated platelets, but it was completely eliminated by extracellular calcium chelators or inhibitors of platelet activation. These studies show the existence of 2 distinct pathways regulating the procoagulant function of platelets. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Arachiche, D. Kerbiriou-Nabias, I. Garcin, T. Letellier, and J. Dachary-Prigent Rapid Procoagulant Phosphatidylserine Exposure Relies on High Cytosolic Calcium Rather Than on Mitochondrial Depolarization Arterioscler Thromb Vasc Biol, November 1, 2009; 29(11): 1883 - 1889. [Abstract] [Full Text] [PDF]

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