ON THE ROLE OF VON-WILLEBRAND-FACTOR IN PROMOTING PLATELET-ADHESION TO FIBRIN IN FLOWING BLOOD
ON THE ROLE OF VON-WILLEBRAND-FACTOR IN PROMOTING PLATELET-ADHESION TO FIBRIN IN FLOWING BLOOD
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DOI：
10.1182/blood.v86.11.4158.bloodjournal86114158
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发表时间：
1995-12-01
期刊：
影响因子：
20.3
通讯作者：
DEGROOT, PG
中科院分区：
文献类型：
--
作者：
ENDENBURG, SC;HANTGAN, RR;DEGROOT, PG
在高剪切速率下血小板与纤维蛋白的粘附依赖于糖蛋白（GP）IIb：IIIa复合物和GPIb与血管性血友病因子（VWF）之间的次级相互作用。血小板和vWF之间促进血小板粘附于纤维蛋白的这种替代联系已在流动的全血中用矩形灌注室进行了检查。如以下观察结果所示，最佳粘附需要血小板和vWF。当血浆灌注在纤维蛋白表面或当包被的纤维蛋白原与对照血浆在酶联免疫吸附试验中孵育时，未检测到vWF的结合。然而，当血小板存在于灌注过程中，VWF和纤维蛋白之间的相互作用可以可视化与免疫电镜。在用严重的血管性血友病血液灌注之前，将纤维蛋白表面暴露于正常血浆并不能补偿粘附所必需的血浆VWF的存在。其中GPIIb：IIIa结合位点突变或GPIb结合位点缺失的vWF突变体表明，VWF仅与血小板上的GPIb相互作用以支持与纤维蛋白的粘附，而不与GPIIb：IIIa相互作用。互补的结果，获得了特异性单克隆抗体抗vWF。因此，vWF必须首先与血小板结合，然后才能与纤维蛋白相互作用并促进血小板粘附。此外，只有GPIb，而不是GPIIb：IIIa，直接参与VWF与血小板的相互作用。(C)1995年，美国血液学会。
Platelet adhesion to fibrin at high shear rates depends on both the glycoprotein (GP) IIb:IIIa complex and a secondary interaction between GPIb and von Willebrand factor (VWF). This alternative link between platelets and vWF in promoting platelet adhesion to fibrin has been examined in flowing whole blood with a rectangular perfusion chamber. Optimal adhesion required both platelets and vWF, as shown by the following observations. No binding of vWF could be detected when plasma was perfused over a fibrin surface or when coated fibrinogen was incubated with control plasma in an enzyme-linked immunosorbent assay. However, when platelets were present during perfusion, interactions between VWF and fibrin could be visualized with immunoelectron microscopy. Exposure of fibrin surfaces to normal plasma before perfusion with severe von Willebrand's disease blood did not compensate for the presence of plasma VWF necessary for adhesion. vWF mutants in which the GPIIb:IIIa binding site was mutated or the GPIb binding site was deleted showed that VWF only interacts with GPIb on platelets in supporting adhesion to fibrin and not with GPIIb:IIIa. Complementary results were obtained with specific monoclonal antibodies against vWF. Thus, vWF must first bind to platelets before it can interact with fibrin and promote platelet adhesion. Furthermore, only GPIb, but not GPIIb:IIIa, is directly involved in this interaction of VWF with platelets. (C) 1995 by The American Society of Hematology.