ENHANCEMENT OF MONONUCLEAR PROCOAGULANT ACTIVITY BY PLATELET 12-HYDROXYEICOSATETRAENOIC ACID
ENHANCEMENT OF MONONUCLEAR PROCOAGULANT ACTIVITY BY PLATELET 12-HYDROXYEICOSATETRAENOIC ACID
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DOI：
10.1172/jci112592
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发表时间：
1986-08-01
影响因子：
15.9
通讯作者：
BROEKMAN, MJ
中科院分区：
文献类型：
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作者：
LORENZET, R;NIEMETZ, J;BROEKMAN, MJ
血小板诱导单核白细胞产生促凝组织因子活性（TFa），并增强内毒素诱导的TFa。我们目前的研究表明，花生四烯酸本身对单核TFa没有影响，但却大大增强了血小板诱导的TFa。对血小板和花生四烯酸的影响都是浓度依赖性的（1-20 μ m）；其他测试的脂肪酸则没有活性。如果血小板暴露于阿司匹林，花生四烯酸酯的增强作用更为明显，表明脂氧合酶产物参与其中。在阿司匹林处理的血小板/花生四烯酸酯/单核细胞制剂中，生物化学证明了12-羟基二碳四烯酸（12-HETE）的产生产生高水平的TFa。12-HETE的增强作用验证如下：添加血小板衍生或合成的12-HETE可使内毒素诱导的TFa增加三倍以上。其他脂氧合酶产物无活性。12-HETE对单核细胞TFa的增强代表了这种类二十烷在血小板和单核细胞之间的细胞相互作用中的一种新描述的生物学功能。
Platelets induce generation of procoagulant tissue factor activity (TFa) by mononuclear leukocytes, and also enhance the TFa induced by endotoxin. Our present investigation demonstrated that arachidonic acid, which by itself had no effect on mononuclear TFa, greatly enhanced platelet-induced TFa. The effect was concentration dependent for both platelets and arachidonate (1-20 .mu.M); other fatty acids tested were inactive. The enhancing effect of arachidonate was more pronounced if platelets were exposed to aspirin, suggesting lipoxygenase product involvement. Production of 12-hydroxyeicosatetraenoic acid (12-HETE) was demonstrated biochemicaly in aspirin-treated platelet/arachidonate/mononuclear cell preparations that generated high levels of TFa. The enhancing role of 12-HETE was verified as follows. Addition of platelet-derived or synthetic 12-HETE amplified endotoxin-induced TFa more than threefold. Other lipoxygenase products were inactive. Enhancement of mononuclear cell TFa by 12-HETE represents a newly described biological function for this eicosanoid in cell-cell interactions between platelets and mononuclear cells.