Lorenzet R, Niemetz J, Marcus A J, Broekman M J
J Clin Invest. 1986 Aug;78(2):418-23. doi: 10.1172/JCI112592.
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 microM); 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 biochemically 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.
血小板可诱导单核白细胞产生促凝血组织因子活性(TFa),还能增强内毒素诱导的TFa。我们目前的研究表明,花生四烯酸本身对单核TFa无影响,但能极大地增强血小板诱导的TFa。该效应在血小板和花生四烯酸盐(1-20 microM)方面均呈浓度依赖性;所测试的其他脂肪酸无活性。如果血小板暴露于阿司匹林,花生四烯酸盐的增强作用会更明显,提示脂氧合酶产物参与其中。在产生高水平TFa的阿司匹林处理的血小板/花生四烯酸盐/单核细胞制剂中,通过生化方法证实了12-羟基二十碳四烯酸(12-HETE)的产生。12-HETE的增强作用通过以下方式得到验证。添加血小板衍生的或合成的12-HETE可使内毒素诱导的TFa放大三倍以上。其他脂氧合酶产物无活性。12-HETE对单核细胞TFa的增强作用代表了这种类花生酸在血小板与单核细胞之间的细胞间相互作用中一种新描述的生物学功能。