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首页> 外文期刊>Cytokine >Interleukin-1beta stimulates platelet-activating factor production in U-937 cells modulating both its biosynthetic and catabolic enzymes
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Interleukin-1beta stimulates platelet-activating factor production in U-937 cells modulating both its biosynthetic and catabolic enzymes

机译：白介素1β刺激U-937细胞中的血小板活化因子产生，从而调节其生物合成和分解代谢酶

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Interleukin-1beta (IL-1β) is a potent agonist of platelet-activating factor (PAF) synthesis. The monocyte-derived PAF may amplify the inflammatory and thrombotic processes. The IL-1β-induced enzymatic alterations leading to increased PAF synthesis are ill-defined. In the present study the last enzymatic activities of the remodeling (acetyl-CoA:lyso-PAF acetyltransferase) and de novo (DTT-insensitive CDP-choline:1-alkyl-2-acetyl-sn-glycerol cholinephosphotransferase) biosynthetic routes of PAF and its main catabolic enzyme, PAF acetylhydrolase, along with the intracellular and extracellular PAF levels were determined in homogenates and medium of U-937 after their stimulation with recombinant IL-1β. IL-1β at 2.5. ng/mL induced an early (0.5-3. h) and a late (12. h) elevation of intracellular PAF levels (2-fold). Only a small portion of intracellular PAF (~10%) was released to the extracellular medium. IL-1β increased lyso-PAF acetyltrasnferase activity which was peaked at 3. h and kept elevated till 12. h. A rapid 1.5-fold increase of cholinephosphotransferase activity was observed in IL-1β stimulated cells. Finally, a transient stimulation of intracellular PAF-AH was induced by IL-1β at 3. h while incubation of U-937 with the PAF acetylhydrolase inhibitor pefabloc in the presence or absence of IL-1β led to a strong sustained increase of intracellular PAF levels. In conclusion, both biosynthetic routes of PAF, along with its degradation can be modulated by IL-1β in a time-specific manner. The inhibition of PAF acetylhydrolase strongly augments PAF's intracellular levels implying its crucial role for the regulation of cellular PAF. The regulation of PAF's enzymatic machinery under inflammatory conditions is more complicated than we thought to be.
机译：白细胞介素-1β（IL-1β）是血小板活化因子（PAF）合成的有效激动剂。单核细胞衍生的PAF可能会加剧炎症和血栓形成过程。 IL-1β诱导的导致PAF合成增加的酶促改变尚不清楚。在本研究中，重塑（乙酰辅酶A：溶血PAF乙酰转移酶）和从头（DTT不敏感的CDP-胆碱：1-烷基-2-乙酰基-sn-甘油胆碱磷酸转移酶）的生物合成途径的最后酶活性在重组IL-1β刺激后，在U-937的匀浆和培养基中测定了其主要分解代谢酶PAF乙酰水解酶以及细胞内和细胞外PAF水平。 IL-1β为2.5。 ng / mL引起细胞内PAF水平的早期升高（0.5-3。h）和晚期（12. h）（2倍）。细胞内PAF中只有一小部分（〜10％）被释放到细胞外培养基中。 IL-1β增加了溶血-PAF乙酰转移酶的活性，该活性在3. h达到峰值，并保持升高直至12 h。在IL-1β刺激的细胞中，胆碱磷酸转移酶活性迅速增加了1.5倍。最后，IL-1β在3. h诱导细胞内PAF-AH的短暂刺激，而在存在或不存在IL-1β的情况下将U-937与PAF乙酰水解酶抑制剂pefabloc一起孵育会导致细胞内PAF的持续强力增加水平。总之，IL-1β可以以时间特异性方式调节PAF的两种生物合成途径及其降解。对PAF乙酰水解酶的抑制作用会大大增强PAF的细胞内水平，这暗示其对于调节细胞PAF的关键作用。在炎症条件下对PAF酶机制的调节比我们想象的要复杂。

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