Role of complement C9 and calcium in the generation of arachidonic acid and its metabolites from rat polymorphonuclear leukocytes.
Role of complement C9 and calcium in the generation of arachidonic acid and its metabolites from rat polymorphonuclear leukocytes.
复制标题
补体 C9 和钙在大鼠多形核白细胞生成花生四烯酸及其代谢物中的作用。
DOI：
10.1016/0161-5890(87)90120-9
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发表时间：
1987
影响因子：
3.6
通讯作者：
Ramm,LE
中科院分区：
文献类型：
--
作者：
Imagawa,DK;Barbour,SE;Morgan,BP;Wright,TM;Shin,HS;Ramm,LE
我们以前已经表明，抗体致敏的小鼠腹腔巨噬细胞释放花生四烯酸（C20：4）和它的含氧衍生物处理时，与补体，和释放的主要部分依赖于终端补体复合物（TCC）。为了进一步描述负责这种释放的过程，我们将我们的研究扩展到大鼠腹膜多形核白细胞（PMNs）。用[3 H]C20：4标记的抗体致敏的大鼠中性粒细胞进行实验，并携带TCC、C5 b-7、C5 b-8或C5 b-9。与其他研究结果相反，主要放射性标记衍生物白三烯B4（LTB 4）的产生严格依赖于C9的存在。然而，在C5 b-9阶段之前产生低水平的C20：4和洋地黄素（PGs）。动力学研究表明，LTB 4的释放是迅速的，初始释放发生在4-6分钟内，第二次释放的上升与细胞死亡相一致。几乎所有的LTB 4产生的释放，因为我们没有发现证据的细胞内的LTB 4保留在C5 b-8或C5 b-9阶段。在细胞外钙缺乏的情况下，LTB 4的释放完全消失，C20：4和PGs的释放急剧减少。[3 H]C20：4标记的携带C5 b-9的PMN在EGTA存在下确实释放了大量放射性标记物质;然而，这种脂质的大部分以完整磷脂和甘油三酯的形式存在。这些结果表明，大鼠PMNs释放C20：4及其含氧衍生物是（1）依赖于C9参与细胞膜上预先存在的C5 b-8复合物，（2）主要依赖于钙的存在。
We have previously shown that antibody-sensitized mouse peritoneal macrophages release arachidonic acid (C20:4) and its oxygenated derivatives when treated with complement, and that the major part of the release depended on the terminal complement complexes (TCC). To further delineate the process(es) responsible for this release we have extended our studies to rat peritoneal poly-morphonuclear leukocytes (PMNs). Experiments were performed with antibody-sensitized rat PMNs labeled with [3H]C20:4 and carrying the TCC, C5b-7, C5b-8 or C5b-9. In contrast to the results of other studies, production of leukotriene B4(LTB4), the major radiolabeled derivative, was strictly dependent on the presence of C9. However, low levels of C20:4 and prostaglandins (PGs) were produced prior to the C5b-9 stage. Kinetic studies demonstrated that release of LTB4was rapid; the initial release occurred within 4–6 min and a second rise in release coincided with cell death. Virtually all the LTB4produced was released as we found no evidence of retention of intracellular LTB4at either the C5b-8 or C5b-9 stages. In the absence of extracellular calcium, the release of LTB4was completely abolished and the release of C20:4 and PGs was drastically reduced. [3H]C20:4-labeled PMNs carrying C5b-9 did release substantial amounts of radiolabeled material in the presence of EGTA; however, the majority of this lipid was in the form of intact phospholipid and triglyceride. These results indicate that release of C20:4 and its oxygenated derivatives from rat PMNs is (1) dependent on the participation ofC9 in the preexisting C5b-8 complex in the cell membrane, and (2) largely dependent on the presence of calcium.