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Blood, 1 April 2006, Vol. 107, No. 7, pp. 2753-2758. Prepublished online as a Blood First Edition Paper on December 8, 2005; DOI 10.1182/blood-2005-09-3755. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-09-3755v1 107/7/2753    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 Giri, T. K. Articles by Tollefsen, D. M. Search for Related Content PubMed PubMed Citation Articles by Giri, T. K. Articles by Tollefsen, D. M. Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Placental dermatan sulfate: isolation, anticoagulant activity, and association with heparin cofactor II Tusar K. Giri, and Douglas M. Tollefsen From the Hematology Division, Department of Medicine, Washington University Medical School, St Louis, MO. Pregnancy is associated with hemostatic challenges that may lead to thrombosis. Heparin cofactor II (HCII) is a glycosaminoglycan-dependent thrombin inhibitor present in both maternal and fetal plasma. HCII activity increases during pregnancy, and HCII levels are significantly decreased in women with severe pre-eclampsia. Dermatan sulfate (DS) specifically activates HCII and is abundant in the placenta, but the locations of DS and HCII in the placenta have not been determined. We present evidence that DS is the major anticoagulant glycosaminoglycan in the human placenta at term. DS isolated from human placenta contains disaccharides implicated in activation of HCII and has anticoagulant activity similar to that of mucosal DS. Immunohistochemical studies revealed that DS is associated with fetal blood vessels and stromal regions of placental villi but is notably absent from the syncytiotrophoblast cells in contact with the maternal circulation. HCII colocalizes with DS in the walls of fetal blood vessels and is also present in syncytiotrophoblast cells. Our data suggest that DS is in a position to activate HCII in the fetal blood vessels or in the stroma of placental villi after injury to the syncytiotrophoblast layer and thereby inhibit fibrin generation in the placenta. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: L. He, T. K. Giri, C. P. Vicente, and D. M. Tollefsen Vascular dermatan sulfate regulates the antithrombotic activity of heparin cofactor II Blood, April 15, 2008; 111(8): 4118 - 4125. [Abstract] [Full Text] [PDF] D. M. Tollefsen Heparin Cofactor II Modulates the Response to Vascular Injury Arterioscler. Thromb. Vasc. Biol., March 1, 2007; 27(3): 454 - 460. [Abstract] [Full Text] [PDF]

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