当降解酶乙酰水解酶被阻断时，凝血酶刺激的人血小板会产生血小板激活因子（1-O-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）。

Human platelets stimulated by thrombin produce platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) when the degrading enzyme acetyl hydrolase is blocked.

作者信息

Touqui L, Hatmi M, Vargaftig B B

出版信息

Biochem J. 1985 Aug 1;229(3):811-6. doi: 10.1042/bj2290811.

DOI:10.1042/bj2290811

PMID:4052028

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1145129/

Abstract

It has been shown [Touqui, Jacquemin & Vargaftig (1983) Thromb. Haemostasis 50, 163; Touqui, Jacquemin & Vargaftig (1983) Biochem. Biophys. Res. Commun. 110, 890-893; Alam, Smith & Melvin (1983) Lipids 18, 534-538; Pieroni & Hanahan (1983) Arch. Biochem. Biophys. 224, 485-493] that rabbit platelets inactivate exogenous PAF (platelet-activating factor, PAF-acether) by a deacetylation-reacylation mechanism. The deacetylation step is catalysed by an acetyl hydrolase sensitive to the serine-hydrolase inhibitor PMSF (phenylmethanesulphonyl fluoride) [Touqui, Jacquemin, Dumarey & Vargaftig (1985) Biochim. Biophys. Acta 833, 111-118]. We report here that human platelets can produce PAF on thrombin stimulation. This production is marginal and transient, reaching a maximum at 10 min and decreasing thereafter. In contrast, 10-12 times more PAF is produced when platelets are treated with PMSF and stimulated with thrombin. Under these conditions, the maximum formation is observed at 30 min and no decline occurs for up to 60 min after stimulation. In addition, these platelets (treated with PMSF and stimulated with thrombin) incorporate exogenous labelled acetate in the 2-position of PAF, probably by an acetyltransferase-dependent mechanism. Production of PAF by human platelets during physiological stimulation can be demonstrated when PAF degradation is suppressed by the acetyl-hydrolase inhibitor PMSF.

摘要

已有研究表明 [图基、雅克曼 & 瓦尔加夫蒂格（1983年）《血栓与止血》50卷，第163页；图基、雅克曼 & 瓦尔加夫蒂格（1983年）《生物化学与生物物理学研究通讯》110卷，第890 - 893页；阿拉姆、史密斯 & 梅尔文（1983年）《脂质》18卷，第534 - 538页；皮耶罗尼 & 哈纳汉（1983年）《生物化学与生物物理学档案》224卷，第485 - 493页]，兔血小板通过脱乙酰化 - 再酰化机制使外源性PAF（血小板活化因子，PAF - 乙醚）失活。脱乙酰化步骤由对丝氨酸水解酶抑制剂PMSF（苯甲基磺酰氟）敏感的乙酰水解酶催化 [图基、雅克曼、迪马雷 & 瓦尔加夫蒂格（1985年）《生物化学与生物物理学学报》833卷，第111 - 118页]。我们在此报告，人血小板在凝血酶刺激下可产生PAF。这种产生量较少且短暂，在10分钟时达到最大值，此后下降。相比之下，当血小板用PMSF处理并经凝血酶刺激时，产生的PAF多10 - 12倍。在这些条件下，在30分钟时观察到最大生成量，刺激后长达60分钟都没有下降。此外，这些（用PMSF处理并经凝血酶刺激的）血小板可能通过依赖乙酰转移酶的机制将外源性标记乙酸掺入PAF的2位。当乙酰水解酶抑制剂PMSF抑制PAF降解时，可证明人血小板在生理刺激过程中产生PAF。

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Human platelets stimulated by thrombin produce platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) when the degrading enzyme acetyl hydrolase is blocked.当降解酶乙酰水解酶被阻断时，凝血酶刺激的人血小板会产生血小板激活因子（1-O-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）。

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