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Blood, 1 January 2004, Vol. 103, No. 1, pp. 152-154. Prepublished online as a Blood First Edition Paper on September 22, 2003; DOI 10.1182/blood-2003-08-2707. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-08-2707v1 103/1/152    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 Camerer, E. Articles by Coughlin, S. R. Search for Related Content PubMed PubMed Citation Articles by Camerer, E. Articles by Coughlin, S. R. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Combined deficiency of protease-activated receptor-4 and fibrinogen recapitulates the hemostatic defect but not the embryonic lethality of prothrombin deficiency Eric Camerer, Daniel N. Duong, Justin R. Hamilton, and Shaun R. Coughlin From the Cardiovascular Research Institute, University of California, San Francisco. The availability of the relevant mutant mouse lines provided an opportunity to test the doctrine that platelet activation and fibrin formation account for the importance of thrombin for hemostasis. Prothrombin-deficient mice that survive to birth exsanguinate in the perinatal period. By contrast, protease-activated receptor 4 (PAR4)–deficient mice, which have platelets that fail to respond to thrombin, survive to adulthood with only a mild bleeding diathesis, and fibrinogen-deficient mice show perinatal bleeding but those that survive this period can have a relatively normal life expectancy. We now report that mice that lacked both PAR4 and fibrinogen exsanguinated at birth like prothrombin-deficient mice. However, while approximately half of prothrombindeficient embryos die during midgestation, mice lacking both PAR4 and fibrinogen developed normally. At face value, these results suggest that platelet activation and fibrin formation are together sufficient to account for the importance of thrombin for hemostasis but not for its importance for embryonic development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: N. Mackman Bleeding hearts Blood, January 15, 2009; 113(3): 500 - 501. [Full Text] [PDF] R. Sood, L. Sholl, B. Isermann, M. Zogg, S. R. Coughlin, and H. Weiler Maternal Par4 and platelets contribute to defective placenta formation in mouse embryos lacking thrombomodulin Blood, August 1, 2008; 112(3): 585 - 591. [Abstract] [Full Text] [PDF] N. Mackman Tissue-Specific Hemostasis in Mice Arterioscler Thromb Vasc Biol, November 1, 2005; 25(11): 2273 - 2281. [Abstract] [Full Text] [PDF] M. J. Ludeman, H. Kataoka, Y. Srinivasan, N. L. Esmon, C. T. Esmon, and S. R. Coughlin PAR1 Cleavage and Signaling in Response to Activated Protein C and Thrombin J. Biol. Chem., April 1, 2005; 280(13): 13122 - 13128. [Abstract] [Full Text] [PDF] N. Mackman Role of Tissue Factor in Hemostasis, Thrombosis, and Vascular Development Arterioscler Thromb Vasc Biol, June 1, 2004; 24(6): 1015 - 1022. [Abstract] [Full Text] [PDF]

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