Emilsson A, Sundler R
Biochim Biophys Acta. 1985 Aug 30;846(2):265-74. doi: 10.1016/0167-4889(85)90074-6.
Exposure of mouse peritoneal macrophages to ionophore A23187 caused a rapid and extensive Ca2+-dependent phospholipid degradation and mobilization of arachidonic acid. Phosphatidylinositol, phosphatidylcholine and phosphatidylethanolamine all contributed to the arachidonic acid release, although the ethanolamine phospholipids incorporated [3H]arachidonic acid more slowly during the prelabeling period, particularly the plasmalogen form. Several enzymatic pathways could be positively identified as contributing to the ionophore-induced phospholipid degradation by the use of several different radiolabeled phospholipid precursors: (i) a phospholipase A-mediated deacylation, (ii) a phosphodiesterase (phospholipase C) reaction, rapidly generating diacylglycerol units from inositol phospholipids, and (iii) enzymatic processes generating diacylglycerol and CDP- and phosphocholine/ethanolamine from phosphatidylcholine/ethanolamine. The diacylglycerol formed was in part phosphorylated and in part hydrolyzed to monoacylglycerol, with retention of its arachidonic acid. These, and other, results indicate that the Ca2+-ionophore activates several apparently distinct phospholipid-degrading processes, in contrast to stimuli acting via cellular receptors.
将小鼠腹腔巨噬细胞暴露于离子载体A23187会导致快速且广泛的Ca2+依赖性磷脂降解以及花生四烯酸的动员。磷脂酰肌醇、磷脂酰胆碱和磷脂酰乙醇胺均参与了花生四烯酸的释放，尽管在预标记期间乙醇胺磷脂掺入[3H]花生四烯酸的速度较慢，尤其是缩醛磷脂形式。通过使用几种不同的放射性标记磷脂前体，可以明确几种酶促途径对离子载体诱导的磷脂降解有作用：(i) 磷脂酶A介导的脱酰基作用；(ii) 磷酸二酯酶（磷脂酶C）反应，迅速从肌醇磷脂生成二酰基甘油单元；(iii) 从磷脂酰胆碱/乙醇胺生成二酰基甘油、CDP-和磷酸胆碱/乙醇胺的酶促过程。形成的二酰基甘油部分被磷酸化，部分水解为单酰基甘油，同时保留其花生四烯酸。这些以及其他结果表明，与通过细胞受体起作用的刺激物相反，Ca2+离子载体激活了几个明显不同的磷脂降解过程。
