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首页> 外文期刊>Journal of Cellular Physiology >Ca2+ influx, phosphoinositide hydrolysis, and histamine release induced by lysophosphatidylserine in mast cells.
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Ca2+ influx, phosphoinositide hydrolysis, and histamine release induced by lysophosphatidylserine in mast cells.

机译：Ca2 +涌入,磷酸肌醇水解组胺释放引起的lysophosphatidylserine肥大细胞。

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摘要

We have previously demonstrated that snake venom phospholipases A2 (PLA2s) and mammalian PLA2s induced inflammatory processes. This effect was correlated with the activity of the enzymes and the release of lipid mediators. We have now determined the role of lysophosphatidylserine (LysoPS) as an inflammatory lipid mediator. Thus, we have studied the possibility that intracellular calcium concentration, phosphoinositide hydrolysis, and the subsequent histamine release in mast cells is due to the action of lysophosphatidylserine. Lysophosphatidylserine-stimulated release of histamine was significantly higher than release by other lysophospholipids. The contribution of increased phospholipase C activity and the intracellular Ca2+ influx were therefore examined. LysoPS increased mast cell calcium concentration, and this increment was associated with phospholipase C activation and release of inositol phosphates. The increase in intracellular calcium and histamine degranulation induced by LysoPS were inhibited by apomorphine. Pretreatment of mast cells with pertussis toxin decreased the secretagogic effect of LysoPS and compound 48/80 without modifying the effect of the ionophore A23187. These results suggest that pertussis toxin-sensitive G-protein might be involved in the mast cell degranulation produced by lysophosphatidylserine and allow the increase in phospholipase C activity, thus enhancing intracellular calcium concentration, which then induces exocytosis of histamine.
机译：我们曾表明蛇毒磷脂酶A2 (PLA2s)和哺乳动物PLA2s诱导炎症过程。与酶的活动脂质介质的释放。确定lysophosphatidylserine的角色(LysoPS)作为炎症性脂质中介。我们研究过的可能性细胞内钙离子浓度,磷酸肌醇水解,随后在肥大细胞组胺释放是由于lysophosphatidylserine的行动。Lysophosphatidylserine-stimulated释放组胺是明显高于释放其他的溶血。磷脂酶C活动和增加因此,细胞内钙离子涌入检查。浓度,增加有关磷脂酶C激活和释放肌醇磷酸盐。细胞内钙和组胺脱粒引起LysoPS被阿朴吗啡抑制。预处理的肥大细胞百日咳毒素LysoPS secretagogic效应和减少化合物48/80没有修改的影响的离子载体A23187。百日咳toxin-sensitive蛋白参与了肥大细胞脱粒lysophosphatidylserine和允许增加磷脂酶C活动,从而增强细胞内钙离子浓度,然后组胺诱导胞外分泌。

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