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首页> 外文期刊>Life sciences >Characteristics of lysophosphatidylcholine-induced Ca2+ response in human neuroblastoma SH-SY5Y cells.
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Characteristics of lysophosphatidylcholine-induced Ca2+ response in human neuroblastoma SH-SY5Y cells.

机译：人神经母细胞瘤SH-SY5Y细胞中溶血磷脂酰胆碱诱导的Ca2 +响应的特征。

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摘要

Lysophosphatidylcholine (LPC) is an important bioactive lipid. In the nervous system, elevated levels of LPC have been shown to produce demyelination. In the present study, we examined the effect of exogenous LPC on intracellular Ca2+ mobilization in human neuroblastoma SH-SY5Y cells. In Ca2+-containing medium, introduction of LPC induced a steady rise in cytosolic Ca2+ levels ([Ca2+]i) in a dose-dependent manner, and this rise was provoked by LPC itself, not by its hydrolysis product produced by lysophospholipase. The increase in [Ca2+]i was reduced by 36% by removal of extracellular Ca2+, while preincubation of the cells with verapamil, an L-type Ca2+ channel blocker, inhibited the response by 23%, part of the Ca2+ influx. Conversely, Ni2+, which inhibits the Na+-Ca2+ exchanger, or Na+-deprivation did not affect LPC-induced Ca2+ influx. In Ca2+-free medium, depletion of Ca2+ stores in the endoplasmic reticulum (ER) by thapsigargin, an ER Ca2+-ATPase inhibitor, abolished the Ca2+ increase. Moreover, LPC-induced [Ca2+]i increase was fully blocked by ruthenium red and procaine, inhibitors of ryanodine receptor (RyR), but was not affected by 2-aminoethoxydiphenyl borate, an inhibitor of inositol triphosphate receptor, or by pertussis toxin, a G(i/o) protein inhibitor. Combined treatment with verapamil plus thapsigargin markedly inhibited but did not abolish the LPC-induced Ca2+ response. These findings indicate that LPC-induced [Ca2+]i increase depends on both external Ca2+ influx and Ca2+ release from ER Ca2+ stores, in which L-type Ca2+ channels and RyRs may be involved. However, in digitonin-permeabilized SH-SY5Y cells, LPC could not induce any [Ca2+]i increase in Ca2+-free medium, suggesting that LPC may act indirectly on RyRs of ER.
机译：溶血磷脂酰胆碱（LPC）是重要的生物活性脂质。在神经系统中，LPC水平升高已显示出脱髓鞘。在本研究中，我们检查了外源LPC对人神经母细胞瘤SH-SY5Y细胞内Ca2 +动员的影响。在含Ca2 +的培养基中，LPC的引入以剂量依赖的方式诱导了胞浆Ca2 +水平（[Ca2 +] i）的稳定上升，而这种上升是LPC本身引起的，而不是由溶血磷脂酶产生的水解产物引起的。通过去除细胞外Ca2 +，[Ca2 +] i的增加减少了36％，而将细胞与维拉帕米（一种L型Ca2 +通道阻滞剂）一起预温育则抑制了23％（部分Ca2 +流入）的反应。相反，抑制Na + -Ca2 +交换子或Na +剥夺的Ni2 +不会影响LPC诱导的Ca2 +流入。在不含Ca2 +的培养基中，thapsigargin（一种ER Ca2 + -ATPase抑制剂）耗尽了内质网（ER）中的Ca2 +，从而消除了Ca2 +的增加。此外，LPC诱导的[Ca2 +] i的增加完全被钌红和普鲁卡因（瑞丹碱受体（RyR）的抑制剂）完全阻滞，但不受2-氨基乙氧基二苯基硼酸酯（肌醇三磷酸受体的抑制剂）或百日咳毒素（a G（i / o）蛋白抑制剂。维拉帕米加毒胡萝卜素的联合治疗显着抑制但并未消除LPC诱导的Ca2 +反应。这些发现表明，LPC诱导的[Ca2 +] i的增加取决于外部Ca2 +流入量和ER Ca2 +存储区中Ca2 +的释放，其中可能涉及L型Ca2 +通道和RyRs。然而，在经过洋地黄素渗透的SH-SY5Y细胞中，LPC不能在无Ca2 +的培养基中诱导任何[Ca2 +] i的增加，这表明LPC可能间接作用于ER的RyRs。

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