title: Tissue factor pathway vs. collagen pathway for in vivo platelet activation.
abstract: The roles that the various platelet collagen receptors play in initial platelet adhesion and thrombus growth remain controversial. Here we summarize some of the pertinent data and discuss some recent studies of the initiation and propagation of platelet accumulation into thrombi and the initiation and propagation of thrombin generation. Mice lacking platelet surface glycoprotein VI (GPVI) form normal thrombi in the laser injury model but have a diminished thrombotic response to severe FeCl3 injury. We hypothesize that the paths to thrombus formation in these two models are different with interaction of GPVI and collagen predominant early after severe FeCl3-induced injury but platelet activation by thrombin predominant after laser-induced injury. Understanding of the response to insult in thrombosis models deepens our understanding of the process and provides a firm foundation for evaluation of anti-thrombotic therapy in these models.
authors.affiliation: Division of Hemostasis and Thrombosis, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA. bfuriel@caregroup.harvard.edu
authors.forename: Barbara C
authors.initials: BC
authors.lastname: Furie
authors.forename: Bruce
authors.initials: B
authors.lastname: Furie
mesh_terms: D000818:Animals; D003094:Collagen / Q000378:metabolism*; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism; D051379:Mice; D008954:Models, Biological; D015539:Platelet Activation; D013925:Thromboplastin / Q000378:metabolism*; D013927:Thrombosis / Q000209:etiology
chemical_list: D008565:Membrane Proteins; D003094:Collagen; D013925:Thromboplastin