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Regulation of calcium signalling by 1-O-alkylglycerols in human Jurkat T lymphocytes

机译:1-O-烷基甘油对人Jurkat T淋巴细胞钙信号的调节

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We studied the role of natural occurring 1-O-alkylglycerols on the calcium signalling in Jurkat T-cells. Alkylglycerols evoked an increase in free intracellular calcium concentration [Ca2+]i, in a dose-dependent manner. When the experiments were performed in calcium-free buffer, the alkylglycerol response on the rise of [Ca2+]i was wholly abolished compared with the one in calcium-containing buffer, suggesting that these etherlipids induce a calcium influx by the opening of Ca2+ channels. We further employed inhibitors of voltage-gated calcium channels. We observed that omega-conotoxin, a blocker of N-type voltage-activated Ca2+ channels, but not verapamil, a blocker of L-type voltage-activated Ca2+ channels, curtailed significantly the calcium rise evoked by the lipid agents. Alkylglycerols also induced plasma membrane depolarisation, known to be involved in the opening of the voltage-gated calcium channels. Our study shows that alkylglycerols increase [Ca2+]i influx in human Jurkat T-cells possibly by modulating the permeability of calcium channels. (C) 2004 Elsevier Inc. All rights reserved. [References: 27]
机译:我们研究了天然存在的1-O-烷基甘油对Jurkat T细胞中钙信号传导的作用。烷基甘油以剂量依赖的方式引起游离细胞内钙浓度[Ca2 +] i的增加。当在不含钙的缓冲液中进行实验时,与含钙的缓冲液相比,[Ca2 +] i升高时烷基甘油的反应被完全消除,这表明这些醚脂通过打开Ca2 +通道而引起钙内流。我们进一步采用了电压门控钙通道抑制剂。我们观察到ω-芋螺毒素(一种N型电压激活的Ca2 +通道的阻滞剂)但不是维拉帕米(一种L型电压激活的Ca2 +通道的阻滞剂)显着减少了脂质剂引起的钙升高。烷基甘油还诱导质膜去极化,这已知与电压门控钙通道的开放有关。我们的研究表明,烷基甘油可能通过调节钙通道的通透性来增加人Jurkat T细胞中[Ca2 +] i的流入。 (C)2004 Elsevier Inc.保留所有权利。 [参考:27]

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