Wise H, Xie Z H
Department of Pharmacology, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, NT Hong Kong.
Prostaglandins Leukot Essent Fatty Acids. 1996 Mar;54(3):199-205. doi: 10.1016/s0952-3278(96)90017-4.
The effect of prostaglandins on neutrophil activation has been studied using the human promyelocytic leukemic cell line HL-60, differentiated with dimethyl sulfoxide (DMSO). Prostaglandin E(2) (PGE(2)) directly stimulated HL-60 cell aggregation with an EC(50) value of 30 nM. Studies with prostanoid receptor-selective agonists suggest that the activation of HL-60 cells by PGE(2) was mediated via the EP(2) receptor. Human neutrophils did not aggregate in response to PGE(2), but PGE(2) inhibited the N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated increase in intracellular calcium ([Ca(2+)i]) in both neutrophils and HL-60 cells. In contrast with the aggregation response to FMLP the aggregation response of HL-60 cells to PGE(2) was independent of extracellular calcium and did not involve mobilization of intracellular calcium.
利用经二甲基亚砜（DMSO）诱导分化的人早幼粒白血病细胞系HL-60，研究了前列腺素对中性粒细胞活化的影响。前列腺素E2（PGE2）直接刺激HL-60细胞聚集，其半数有效浓度（EC50）值为30 nM。使用前列腺素受体选择性激动剂进行的研究表明，PGE2对HL-60细胞的活化是通过EP2受体介导的。人中性粒细胞对PGE2无聚集反应，但PGE2可抑制中性粒细胞和HL-60细胞中N-甲酰甲硫氨酰亮氨酰苯丙氨酸（FMLP）刺激引起的细胞内钙浓度（[Ca2+]i）升高。与对FMLP的聚集反应不同，HL-60细胞对PGE2的聚集反应不依赖细胞外钙，也不涉及细胞内钙的动员。
