Ozaki Y, Matsumoto Y, Yatomi Y, Higashihara M, Kume S
Department of Clinical and Laboratory Medicine, Yamanashi Medical College, Japan.
Eur J Biochem. 1991 Jul 15;199(2):347-54. doi: 10.1111/j.1432-1033.1991.tb16130.x.
Arachidonic acid mobilization in platelets activated by low concentrations (less than or equal to 1.6 micrograms/ml) of TP 82, a monoclonal antibody against CD9, appears to consist of two distinct phases. In the first phase, limited arachidonic acid release occurs concomitantly with a shape change induced by TP 82. This appears to be dependent upon phospholipase A2 activation, since it is well preserved in the presence of aspirin, which completely blocked both intracellular Ca2+ elevation and phosphatidic acid formation which would indicate phospholipase C activation. The Na+ Exchange was also found to participate in the first phase of arachidonic acid mobilization, since extracellular Na+ depletion and ethylisopropylamiloride, a specific inhibitor of the Na+/H+ exchanger, effectively blocked this limited mobilization of arachidonic acid. The second, much larger, phase of arachidonic acid mobilization occurs with the beginning of platelet aggregation. A limited amount of thromboxane A2 formed during the first phase of arachidonic acid release plays an important role in induction of the massive arachidonic mobilization in the second phase. Factors, as yet unidentified, also appear to work synergistically with thromboxane A2 to induce the full picture of arachidonic acid mobilization.
低浓度（小于或等于1.6微克/毫升）的抗CD9单克隆抗体TP 82激活血小板后，花生四烯酸的动员似乎由两个不同阶段组成。在第一阶段，有限的花生四烯酸释放与TP 82诱导的形态变化同时发生。这似乎依赖于磷脂酶A2的激活，因为在阿司匹林存在的情况下它得到了很好的保留，阿司匹林完全阻断了细胞内Ca2+升高和磷脂酸形成，而这表明磷脂酶C被激活。还发现Na+交换参与了花生四烯酸动员的第一阶段，因为细胞外Na+耗竭和Na+/H+交换体的特异性抑制剂乙基异丙基氨氯地平有效地阻断了花生四烯酸的这种有限动员。花生四烯酸动员的第二个、大得多的阶段随着血小板聚集的开始而发生。在花生四烯酸释放的第一阶段形成的少量血栓素A2在诱导第二阶段大量花生四烯酸动员中起重要作用。尚未确定的因素似乎也与血栓素A2协同作用，以诱导花生四烯酸动员的全貌。
