Emilsson A, Sundler R
Biochim Biophys Acta. 1986 May 21;876(3):533-42. doi: 10.1016/0005-2760(86)90041-x.
Inositol phospholipid degradation and release of phospholipid-bound arachidonic acid was induced in intact peritoneal macrophages by exposure to phorbol myristate acetate (PMA) or zymosan particles. PMA, known to activate protein kinase C, selectively enhanced the deacylation of phosphatidylinositol (i.e., degradation by phospholipase A), while zymosan particles enhanced degradation via both phospholipase A and inositol lipid phosphodiesterase (phospholipase C). The release of arachidonic acid was found to correlate with the degradation of phosphatidylinositol by the phospholipase A pathway and could be dissociated from the phospholipase C-catalyzed cleavage of inositol phospholipids in several experimental situations: (i) when PMA was the stimulus, (ii) by the difference in Ca2+ dependence between the two enzymatic processes when zymosan was the stimulus and (iii) by the parallel inhibition by chlorpromazine of the phospholipase A pathway and arachidonic acid release, but not inositol phospholipid phosphodiesterase. In addition, phloretin, a reported inhibitor of protein kinase C, was found to inhibit arachidonic acid release and the deacylation of phosphatidylinositol. The results are consistent with a model in which arachidonic acid release is mediated by phospholipase(s) A and in which PMA or the phosphodiesterase-catalyzed degradation of phosphoinositides causes activation of the phospholipase A pathway via protein kinase C.
通过暴露于佛波酯肉豆蔻酸酯（PMA）或酵母聚糖颗粒，在完整的腹膜巨噬细胞中诱导肌醇磷脂降解和磷脂结合的花生四烯酸释放。已知PMA可激活蛋白激酶C，它选择性地增强磷脂酰肌醇的脱酰作用（即通过磷脂酶A降解），而酵母聚糖颗粒通过磷脂酶A和肌醇脂质磷酸二酯酶（磷脂酶C）增强降解。发现花生四烯酸的释放与磷脂酶A途径介导的磷脂酰肌醇降解相关，并且在几种实验情况下可与磷脂酶C催化的肌醇磷脂裂解分离：（i）当PMA作为刺激物时；（ii）当酵母聚糖作为刺激物时，两种酶促过程在Ca2+依赖性上的差异；（iii）通过氯丙嗪对磷脂酶A途径和花生四烯酸释放的平行抑制，但对肌醇磷脂磷酸二酯酶无抑制作用。此外，已报道的蛋白激酶C抑制剂根皮素被发现可抑制花生四烯酸释放和磷脂酰肌醇的脱酰作用。这些结果与一个模型一致，即花生四烯酸释放由磷脂酶A介导，并且PMA或磷酸二酯酶催化的磷酸肌醇降解通过蛋白激酶C导致磷脂酶A途径的激活。
