Tissue factor pathway vs. collagen pathway for in vivo platelet activation

被引:11
作者
Furie, BC [1 ]
Furie, B [1 ]
机构
[1] Beth Israel Deaconess Med Ctr, Dept Med, Div Hemostasis & Thrombosis, Boston, MA 02215 USA
[2] Harvard Univ, Sch Med, Boston, MA 02215 USA
关键词
glycoprotein VI; alpha(2)beta(1); alpha(IIb)beta(3); platelets; thrombus formation; tissue factor; collagen; von Willebrand factor; glycoprotein Ib-IX-V; FcR gamma;
D O I
10.1016/j.bcmd.2005.12.010
中图分类号
R5 [内科学];
学科分类号
1002 [临床医学]; 100201 [内科学];
摘要
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. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:135 / 138
页数:4
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