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Blood, 15 October 2005, Vol. 106, No. 8, pp. 2716-2722. Prepublished online as a Blood First Edition Paper on June 14, 2005; DOI 10.1182/blood-2005-01-0406. This Article Full Text (PDF) All Versions of this Article: 2005-01-0406v1 106/8/2716    most recent Alert me when this article is cited Alert me if a correction is posted 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 Li, W. Articles by Esmon, C. T Search for Related Content PubMed PubMed Citation Articles by Li, W. Articles by Esmon, C. T Related Collections Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted January 31, 2005 Accepted June 5, 2005 Extra-embryonic expression of EPCR is essential for embryonic viability Weihong Li, Xunzhen Zheng, Jian-Ming Gu, Gary L Ferrell, Mingming Brady, Naomi L Esmon, and Charles T Esmon* Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA Howard Hughes Medical Institute, Oklahoma City, OK, USA Berlex Biosciences, Richmond, CA, USA Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA Cardiovascular Biology Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, USA; Howard Hughes Medical Institute, Oklahoma City, OK, USA; Department of Pathology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA * Corresponding author; email: Charles-Esmon{at}omrf.ouhsc.edu. The endothelial cell protein C receptor (EPCR) augments protein C activation by the thrombin-thrombomodulin complex. Deletion of the EPCR gene in mice leads to embryonic lethality before embryonic day 10 (E10.0). EPCR is detected in the giant trophoblast cells at the feto-maternal boundary from E7.5 and weakly in embryonic aortic endothelial cells from E13.5, suggesting that extra-embryo EPCR expression may be essential for embryonic viability. Using conditional knock out strategies, we demonstrate that EPCR deficient embryos with EPCR expression on placenta giant trophoblasts can be carried to term and then develop normally. Conversely, EPCR expression in the embryo, without expression in the giant trophoblast cells, does not rescue the mice. In genetically modified mice with low tissue factor activity, EPCR deficiency is not embryonic lethal. As adults, EPCR deficient mice generate more thrombin and activate less protein C in response to procoagulant stimuli. Spontaneous thrombin formation in the deficient animals increases with age. These findings show that extra-embryonic EPCR expression is critical for embryo development. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: It's the trophoblast! Hartmut Weiler Blood 2005 106: 2603. [Full Text] [PDF] This article has been cited by other articles: M. Delvaeye and E. M. Conway Coagulation and innate immune responses: can we view them separately? Blood, September 17, 2009; 114(12): 2367 - 2374. [Abstract] [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] M. Xue, L. March, P. N Sambrook, K. Fukudome, and C. 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