High shear stress can initiate both platelet aggregation and shedding of procoagulant containing microparticles
High shear stress can initiate both platelet aggregation and shedding of procoagulant containing microparticles
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DOI：
10.1182/blood.v88.9.3456.bloodjournal8893456
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发表时间：
1996-11-01
期刊：
影响因子：
20.3
通讯作者：
Fukuhara, S
中科院分区：
文献类型：
--
作者：
Miyazaki, Y;Nomura, S;Fukuhara, S
先前的研究表明，在不添加任何激动剂的情况下，高水平的剪切力可以产生血小板聚集。我们研究了高剪切力是否会引起血小板聚集和微粒从血小板质膜脱落。使用锥板粘度计施加剪切应力，并通过流式细胞术测量微粒形成。结果发现，随着剪切应力持续时间的增加，微粒形成增加。微粒和残余血小板都显示出其表面上的促凝血活性。对剪切力依赖性微粒形成机制的研究表明，在高剪切力条件下，血管性血友病因子（vWF）与血小板糖蛋白Ib的结合、细胞外钙离子内流和血小板钙蛋白酶的激活是产生微粒的必要条件。蛋白激酶C（PKC）的激活促进了剪切力依赖性微粒的形成。肾上腺素不影响微粒的形成，虽然它增强血小板聚集的高剪切力。这些研究结果表明，在动脉粥样硬化的动脉，病理高剪切应力可能发生的网站，可能有助于动脉血栓形成，通过提供和扩大凝血级联反应的催化表面的微粒的局部生成的可能性。(C)1996年，美国血液学会。
Previous studies have demonstrated that a high level of shear stress can produce platelet aggregation without the addition of any agonist. We investigated whether high shear stress could cause both platelet aggregation and shedding of microparticles from the platelet plasma membrane. A cone-plate viscometer was used to apply shear stress and microparticle formation was measured by flow cytometry. It was found that microparticle formation increased as the duration of shear stress increased. Both microparticles and the remnant platelets showed the exposure of procoagulant activity on their surfaces. Investigation of the mechanisms involved in shear-dependent microparticle generation showed that binding of von Willebrand factor (vWF) to platelet glycoprotein Ib, influx of extracellular calcium, and activation of platelet calpain were required to generate microparticles under high shear stress conditions, Activation of protein kinase C (PKC) promoted shear-dependent microparticle formation. Epinephrine did not influence microparticle formation, although it enhanced platelet aggregation by high shear stress. These findings suggest the possibility that local generation of microparticles in atherosclerotic arteries, the site that pathologically high shear stress could occur, may contribute to arterial thrombosis by providing and expanding a catalytic surface for the coagulation cascade. (C) 1996 by The American Society of Hematology.