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Defective thrombus formation in mice lacking coagulation factor XII.

Authors: Renne, T  Pozgajova, M  Gruner, S  Schuh, K  Pauer, HU  Burfeind, P  Gailani, D  Nieswandt, B 
Citation: Renne T, etal., J Exp Med. 2005 Jul 18;202(2):271-81. Epub 2005 Jul 11.
Pubmed: (View Article at PubMed) PMID:16009717
DOI: Full-text: DOI:10.1084/jem.20050664

Blood coagulation is thought to be initiated by plasma protease factor VIIa in complex with the membrane protein tissue factor. In contrast, coagulation factor XII (FXII)-mediated fibrin formation is not believed to play an important role for coagulation in vivo. We used FXII-deficient mice to study the contributions of FXII to thrombus formation in vivo. Intravital fluorescence microscopy and blood flow measurements in three distinct arterial beds revealed a severe defect in the formation and stabilization of platelet-rich occlusive thrombi. Although FXII-deficient mice do not experience spontaneous or excessive injury-related bleeding, they are protected against collagen- and epinephrine-induced thromboembolism. Infusion of human FXII into FXII-null mice restored injury-induced thrombus formation. These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo. The results establish FXII as essential for thrombus formation, and identify FXII as a novel target for antithrombotic therapy.

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CRRD Object Information
CRRD ID: 11041771
Created: 2016-03-29
Species: All species
Last Modified: 2016-03-29
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.