| First Author | Renné T | Year | 2005 |
| Journal | J Exp Med | Volume | 202 |
| Issue | 2 | Pages | 271-81 |
| PubMed ID | 16009717 | Mgi Jnum | J:100529 |
| Mgi Id | MGI:3588806 | Doi | 10.1084/jem.20050664 |
| Citation | Renne T, et al. (2005) Defective thrombus formation in mice lacking coagulation factor XII. J Exp Med 202(2):271-81 |
| abstractText | 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. |
