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在生理剪切速率下,微粒会黏附于I型胶原、纤维蛋白原、血管性血友病因子以及表面固定的血小板。

Microparticles adhere to collagen type I, fibrinogen, von Willebrand factor and surface immobilised platelets at physiological shear rates.

作者信息

Keuren J F W, Magdeleyns E J P, Bennaghmouch A, Bevers E M, Curvers J, Lindhout T

机构信息

Sanquin Blood Bank Southeast Region, Maastricht, The Netherlands.

出版信息

Br J Haematol. 2007 Aug;138(4):527-33. doi: 10.1111/j.1365-2141.2007.06650.x. Epub 2007 Jun 29.

Abstract

Microparticles (MPs), shed during the storage of platelets, support blood coagulation and could be helpful in restoring the haemostatic system in thrombocytopenic patients. The mechanisms by which MPs support haemostasis under flow conditions were investigated. Fluorescent-labelled MPs were perfused at shear rates of 100 and 1000/s over surfaces coated with collagen, fibrinogen, von Willebrand factor (VWF) or surface-adherent platelets. Adhesion was monitored in real-time by fluorescence microscopy. In addition, thrombin-antithrombin (TAT) complex formation was measured in flowing thrombocytopenic blood. MPs attained the capacity to firmly adhere to collagen, VWF, fibrinogen and surface-adherent platelets at high and low shear rate. Antibodies against glycoprotein Ibalpha and alpha(IIb)beta(3) were used to demonstrate the specificities of these interactions. The addition of MPs to thrombocytopenic blood did not affect platelet adhesion. TAT complex formation was increased in the presence of MPs in capillaries coated with fibrinogen, but not on collagen fibres. We confirmed that MPs adhere to a damaged vascular bed in vivo after infusion in denuded arteries in a mouse model. MPs have platelet-like adhering properties and accelerate thrombin generation. These properties strongly support the notion that MPs can be beneficial in maintaining normal haemostasis when platelet function is impaired or reduced, as in thrombocytopenic patients.

摘要

血小板储存过程中释放的微粒(MPs)可促进血液凝固,可能有助于恢复血小板减少症患者的止血系统。本研究探讨了MPs在血流条件下支持止血的机制。将荧光标记的MPs以100和1000/s的剪切速率灌注到包被有胶原蛋白、纤维蛋白原、血管性血友病因子(VWF)或表面黏附血小板的表面。通过荧光显微镜实时监测黏附情况。此外,还测定了流动的血小板减少症血液中凝血酶-抗凝血酶(TAT)复合物的形成。MPs在高剪切速率和低剪切速率下均能牢固黏附于胶原蛋白、VWF、纤维蛋白原和表面黏附血小板。使用针对糖蛋白Ibalpha和α(IIb)β(3)的抗体来证明这些相互作用的特异性。向血小板减少症血液中添加MPs不影响血小板黏附。在包被有纤维蛋白原的毛细血管中,MPs的存在会增加TAT复合物的形成,但在胶原纤维上则不会。我们证实在小鼠模型中,将MPs注入剥脱动脉后,MPs在体内会黏附于受损的血管床。MPs具有类似血小板的黏附特性,并能加速凝血酶的生成。这些特性有力地支持了以下观点:当血小板功能受损或降低时,如在血小板减少症患者中,MPs有助于维持正常止血。

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