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血小板活化因子促进花生四烯酸掺入中性粒细胞的磷脂酰肌醇和磷脂酰胆碱中。

Platelet-activating factor promotes arachidonate incorporation into phosphatidylinositol and phosphatidylcholine in neutrophils.

作者信息

Tou J

出版信息

Biochem Biophys Res Commun. 1985 Mar 29;127(3):1045-51. doi: 10.1016/s0006-291x(85)80050-4.

Abstract

Platelet-activating factor (1-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine, PAF) promotes the incorporation of [1-14C]arachidonic acid most significantly into phosphatidylinositol (PI) and phosphatidylcholine (PC) during the early stages of guinea pig neutrophil-PAF interaction. The stimulation reached a maximum at 10(-7) M and started to decline at 10(-6) M. No changes in the mass of each phospholipid were detected in neutrophils challenged by PAF for 1 to 5 minutes. The stimulation by PAF on the formation of [14C]arachidonoyl-PC but not [14C]arachidonoyl-PI was dependent on the presence of external Ca2+. These results suggest that the increased acylation of PI and PC elicited by PAF is secondary to an increased deacylation of these phospholipids and the mechanisms by which PAF stimulates the deacylation of PI and PC may be different.

摘要

血小板激活因子(1-0-十六烷基-2-乙酰基-sn-甘油-3-磷酸胆碱,PAF)在豚鼠中性粒细胞与PAF相互作用的早期阶段,能最显著地促进[1-14C]花生四烯酸掺入磷脂酰肌醇(PI)和磷脂酰胆碱(PC)。这种刺激在10^(-7) M时达到最大值,在10^(-6) M时开始下降。在PAF刺激1至5分钟的中性粒细胞中,未检测到各磷脂质量的变化。PAF对[14C]花生四烯酰-PC而非[14C]花生四烯酰-PI形成的刺激依赖于细胞外Ca2+的存在。这些结果表明,PAF引起的PI和PC酰化增加是这些磷脂脱酰作用增加的继发结果,且PAF刺激PI和PC脱酰作用的机制可能不同。

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