Cauwenberghs Sandra, Feijge Marion A H, Harper Alan G S, Sage Stewart O, Curvers Joyce, Heemskerk Johan W M
Department of Biochemistry, CARIM, Maastricht University, PO Box 616, 6200 MD Maastricht, The Netherlands.
FEBS Lett. 2006 Oct 2;580(22):5313-20. doi: 10.1016/j.febslet.2006.08.082. Epub 2006 Sep 12.
Platelet activation by potent, Ca(2+)-mobilizing agonists results in shedding of microparticles that are active in coagulation. Here we show that platelets under storage produce procoagulant microparticles in the absence of agonist. Microparticle formation by resting platelets results from alphaIIbbeta3 signaling to destabilization of the actin cytoskeleton in the absence of calpain activation. Integrin-mediated spreading of platelets over fibrinogen similarly results in microparticle formation. After transfusion of stored platelet preparations to thrombocytopenic patients, the microparticles contribute to coagulant activity in vivo.
强效的、可动员钙离子的激动剂激活血小板会导致具有凝血活性的微粒脱落。在此我们表明，储存状态下的血小板在没有激动剂的情况下也会产生促凝血微粒。静息血小板形成微粒是由于在没有钙蛋白酶激活的情况下，αIIbβ3信号传导导致肌动蛋白细胞骨架不稳定。整合素介导的血小板在纤维蛋白原上的铺展同样会导致微粒形成。将储存的血小板制剂输注给血小板减少症患者后，这些微粒在体内有助于凝血活性。
