Complement-independent Ab-induced peroxide lysis of platelets requires 12-lipoxygenase and a platelet NADPH oxidase pathway
Complement-independent Ab-induced peroxide lysis of platelets requires 12-lipoxygenase and a platelet NADPH oxidase pathway
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DOI：
10.1172/jci200420726
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发表时间：
2004-04-01
影响因子：
15.9
通讯作者：
Karpatkin, S
中科院分区：
文献类型：
--
作者：
Nardi, M;Feinmark, SJ;Karpatkin, S
HIV 相关血小板减少症患者的抗血小板 GPIIIa49-66 Ab 通过产生过氧化物和其他活性氧 (ROS) 诱导血小板减少症和血小板碎片。在此，我们报告了功能性血小板 NADPH 氧化酶途径的存在，该途径需要通过血小板 12-脂氧合酶 (12-LO) 途径激活才能破碎血小板。描述了一种新的 Ab 介导机制，其中血小板 12-LO 产物 12(S)-HETE 激活 NADPH 氧化酶途径以产生 ROS。
Antiplatelet GPIIIa49-66 Ab of HIV-related thrombocytopenic patients induces thrombocytopenia and platelet fragmentation by the generation of peroxide and other reactive oxygen species (ROS). Here we report the presence of a functional platelet NADPH oxidase pathway that requires activation by the platelet 12-lipoxygenase (12-LO) pathway to fragment platelets. A new Ab-mediated mechanism is described in which the platelet 12-LO product, 12(S)-HETE activates the NADPH oxidase pathway to generate ROS.