Agwu D E, McPhail L C, Chabot M C, Daniel L W, Wykle R L, McCall C E
Department of Medicine, Wake Forest University Medical Center, Winston-Salem, North Carolina 27103.
J Biol Chem. 1989 Jan 25;264(3):1405-13.
Stimulation of human polymorphonuclear leukocytes (PMN) may result in the metabolism of phospholipids other than phosphoinositides to generate second-messenger intermediary metabolites. We investigated agonist-induced breakdown of 1-O-alkyl-2-acyl-sn-glycero-3-phosphocholine (1-O-alkyl-2-acyl-GPC), which constitutes almost half the diradyl-GPC fraction in human PMN (Mueller, H. W., O'Flaherty, J. T., Green, D. G., Samuel, M. P., and Wykle, R. L. (1984) J. Lipid Res. 25: 383-388), in cells prelabeled with 1-O-[3H] alkyl-2-acyl-GPC. We also utilized normal-phase high pressure liquid chromatography to quantitate the accumulation of diradylglycerols (1-O-alkyl-2-acylglycerols and diacylglycerols) in stimulated PMN. Phorbol-12-myristate-13-acetate (PMA), 1-oleoyl-2-acetyl-sn-glycerol-, calcium ionophore A23187-, and f-methionyl-leucyl-phenylalanine (fMLP) stimulation of PMN resulted in a time- and concentration-dependent hydrolysis of 1-O-[3H]alkyl-2-acyl-GPC and the formation of 1-O-[3H]alkyl-2-acyl-phosphatidic acid (PA) and 1-O-[3H]alkyl-2-acylglycerol. In all cases formation of 1-O-[3H]alkyl-2-acyl-PA preceded that of 1-O-[3H]alkyl-2-acylglycerol. The times between addition of stimulus and appearance of 1-O-[3H] alkyl-2-acylglycerol varied for PMA (40 s at 1.6 microM), A23187 (5 min at 5 microM), and fMLP (30 sec at 1 microM). Preincubation of cells with 1 microgram/ml pertussis toxin (PT) inhibited the breakdown of 1-O-[3H]alkyl-2-acyl-GPC in cells stimulated with 1 microM fMLP, indicating a role for a PT-sensitive G protein with this stimulus. Quantitation of diglycerides as diradylglycerobenzoates in PMN stimulated with PMA (10 min), A23187 (10 min), or fMLP demonstrated marked accumulation of both 1-O-alkyl-2-acylglycerols and diacylglycerols. The highest increases over controls were observed for fMLP (33-fold for 1-O-alkyl-2-acylglycerols and 17-fold for diacylglycerols). In stimulated PMN prelabeled with 1-O-[3H]hexadecyl-2-acyl-GPC and 1-O-alkyl-2-acyl-sn-glycero-3-[32P]phosphocholine, the ratio of 3H to 32P in 1-O-alkyl-2-acyl-PA compared to 1-O-alkyl-2-acyl-GPC suggested the involvement of a phospholipase D in the hydrolysis of 1-O-[3H]-alkyl-2-acyl-GPC. Thus, stimulation of human PMN results in the hydrolysis of 1-O-[3H]alkyl-2-acyl-GPC to yield 1-O-[3H] alkyl-2-acyl-PA and 1-O-[3H]alkyl-2-acylglycerol possibly initiated by activation of a phospholipase D.(ABSTRACT TRUNCATED AT 250 WORDS)
刺激人多形核白细胞(PMN)可能导致除磷酸肌醇外的磷脂代谢,以产生第二信使中间代谢产物。我们研究了激动剂诱导的1-O-烷基-2-酰基-sn-甘油-3-磷酸胆碱(1-O-烷基-2-酰基-GPC)的分解,其在人PMN中几乎占二酰基-GPC部分的一半(穆勒,H. W.,奥弗莱厄蒂,J. T.,格林,D. G.,塞缪尔,M. P.,和怀克尔,R. L.(1984年)《脂质研究杂志》25: 383 - 388),在预先用1-O-[³H]烷基-2-酰基-GPC标记的细胞中进行。我们还利用正相高压液相色谱法来定量受刺激的PMN中二酰基甘油(1-O-烷基-2-酰基甘油和二酰基甘油)的积累。佛波醇-12-肉豆蔻酸酯-13-乙酸酯(PMA)、1-油酰基-2-乙酰基-sn-甘油、钙离子载体A23187和f-甲硫氨酰-亮氨酰-苯丙氨酸(fMLP)对PMN的刺激导致1-O-[³H]烷基-2-酰基-GPC的时间和浓度依赖性水解,并形成1-O-[³H]烷基-2-酰基磷脂酸(PA)和1-O-[³H]烷基-2-酰基甘油。在所有情况下,1-O-[³H]烷基-2-酰基-PA的形成先于1-O-[³H]烷基-2-酰基甘油。添加刺激物与1-O-[³H]烷基-2-酰基甘油出现之间的时间因PMA(1.6微摩尔时为40秒)、A23187(5微摩尔时为5分钟)和fMLP(1微摩尔时为30秒)而异。用1微克/毫升百日咳毒素(PT)对细胞进行预孵育可抑制1微摩尔fMLP刺激的细胞中1-O-[³H]烷基-2-酰基-GPC的分解,表明PT敏感的G蛋白在这种刺激中起作用。对用PMA(10分钟)、A23187(10分钟)或fMLP刺激的PMN中的二酰基甘油作为二酰基甘油苯甲酸酯进行定量,结果显示1-O-烷基-2-酰基甘油和二酰基甘油均有明显积累。fMLP观察到的比对照增加最多(1-O-烷基-2-酰基甘油增加33倍,二酰基甘油增加17倍)。在用1-O-[³H]十六烷基-2-酰基-GPC和1-O-烷基-2-酰基-sn-甘油-3-[³²P]磷酸胆碱预先标记的受刺激PMN中,1-O-烷基-2-酰基-PA与1-O-烷基-2-酰基-GPC中³H与³²P的比率表明磷脂酶D参与了1-O-[³H]-烷基-2-酰基-GPC的水解。因此,刺激人PMN导致1-O-[³H]烷基-2-酰基-GPC水解,产生1-O-[³H]烷基-2-酰基-PA和1-O-[³H]烷基-2-酰基甘油,这可能是由磷脂酶D的激活引发的。(摘要截短至250字)