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Blood, 15 April 2008, Vol. 111, No. 8, pp. 4137-4144. Prepublished online as a Blood First Edition Paper on February 15, 2008; DOI 10.1182/blood-2007-07-101733. This Article Full Text (PDF) All Versions of this Article: blood-2007-07-101733v1 111/8/4137    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 Werneck, C. C Articles by Mecham, R. P Search for Related Content PubMed PubMed Citation Articles by Werneck, C. C Articles by Mecham, R. P Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 24, 2007 Accepted February 1, 2008 Mice lacking the extracellular matrix protein MAGP1 display delayed thrombotic occlusion following vessel injury Claudio C Werneck, Cristina P Vicente, Justin S Weinberg, Adrian Shifren, Richard A Pierce, Thomas J Broekelmann, Douglas M Tollefsen, and Robert P Mecham* Department of Biochemistry, Insitute of Biology, State University of Campinas, Campinas, Sao Paulo, Brazil Department of Cell Biology, Insitute of Biology, State University of Campinas, Campinas, Sao Paulo, Brazil Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, United States Department of Medicine, Washington University School of Medicine, St. Louis, MO, United States * Corresponding author; email: bmecham{at}wustl.edu. Mice lacking the extracellular matrix protein microfibril associated glycoprotein-1 (MAGP1) display delayed thrombotic occlusion of the carotid artery following injury as well as prolonged bleeding from a tail vein incision. Normal occlusion times were restored when recombinant MAGP1 was infused into deficient animals prior to vessel wounding. Blood coagulation was normal in these animals as assessed by activated partial thromboplastin time and prothrombin time. Platelet number was lower in MAGP1-deficient mice, but the platelets showed normal aggregation properties in response to various agonists. MAGP1 was not found in normal platelets or in the plasma of wild-type mice. In ligand blot assays, MAGP1 bound to fibronectin, fibrinogen, and von Willebrand factor, but von Willebrand factor was the only protein of the three that bound to MAGP1 in surface plasmon resonance studies. These findings show that MAGP1, a component of microfibrils and vascular elastic fibers, plays a role in hemostasis and thrombosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. E. Wagenseil and R. P. Mecham Vascular Extracellular Matrix and Arterial Mechanics Physiol Rev, July 1, 2009; 89(3): 957 - 989. [Abstract] [Full Text] [PDF] J. S. Weinbaum, T. J. Broekelmann, R. A. Pierce, C. C. Werneck, F. Segade, C. S. Craft, R. H. Knutsen, and R. P. Mecham Deficiency in Microfibril-associated Glycoprotein-1 Leads to Complex Phenotypes in Multiple Organ Systems J. Biol. Chem., September 12, 2008; 283(37): 25533 - 25543. [Abstract] [Full Text] [PDF]

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