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首页> 外文期刊>Journal of Cellular Physiology >Pharmacological sensitivity of ATP release triggered by photoliberation of inositol-1,4,5-trisphosphate and zero extracellular calcium in brain endothelial cells.
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Pharmacological sensitivity of ATP release triggered by photoliberation of inositol-1,4,5-trisphosphate and zero extracellular calcium in brain endothelial cells.

机译：药物敏感性的ATP释放photoliberation触发的inositol-1 4 5-trisphosphate和零细胞外钙在大脑内皮细胞。

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摘要

Recently, ATP has gained much interest as an extracellular messenger involved in the communication of calcium signals between cells. The mechanism of ATP release is, however, still a matter of debate. In the present study we investigated the possible contribution of connexin hemichannels or ion channels in the release of ATP in GP8, a rat brain endothelial cell line. Release of ATP was triggered by photoactivation of InsP(3) or by reducing the extracellular calcium concentration. Both trigger protocols induced ATP release significantly above baseline. InsP(3)-triggered ATP release was completely blocked by alpha-glycyrrhetinic acid (alpha-GA), the connexin mimetic peptides gap 26 and 27, and the trivalent ions gadolinium and lanthanum. ATP release triggered by zero calcium was, in addition to these substances, also blocked by flufenamic acid (FFA), niflumic acid, and NPPB. Gap 27 selectively blocked zero calcium-triggered ATP release in connexin-43 transfected HeLa cells, while having no effect in wild-type and connexin-32 transfected cells. Of all the agents used, only alpha-GA, FFA and NPPB significantly reduced gap junctional coupling. In conclusion, InsP(3) and zero calcium-triggered ATP release show major similarities but also some differences in their sensitivity to the agents applied. It is suggested that both stimuli trigger ATP release through the same mechanism, which is connexin-dependent, permeable in both directions, potently blocked by connexin mimetic peptides, and consistent with the opening of connexin hemichannels. J. Cell. Physiol. 197: 205-213, 2003Copyright 2003 Wiley-Liss, Inc.
机译：最近,ATP作为获得太大的兴趣细胞外的信使参与细胞间通讯的钙信号。ATP释放的机理是,然而,仍然有争议的问题。调查的可能贡献联接蛋白hemichannels或离子通道在GP8释放ATP,老鼠大脑内皮细胞系。光活化的高级警官(3)或通过减少细胞外钙离子浓度。协议引起ATP释放显著高于基线。完全被alpha-glycyrrhetinic酸(alpha-GA)联接蛋白模拟肽差距2627日,钆和三价离子镧。除了这些物质,也被氟芬那酸(FFA)、尼氟酸,和NPPB。在connexin-43 calcium-triggered ATP释放转染海拉细胞,而没有效果野生型和connexin-32转染细胞。所有使用的代理,只有alpha-GA、FFA和NPPB显著减少差距联接的耦合。结论,InsP calcium-triggered(3)和零ATP释放显示主要的相似之处,但是也有他们对代理的敏感性的差异应用。触发ATP释放通过相同的机制,connexin-dependent,渗透在两个吗方向,强有力地被联接蛋白模拟肽和一致的开放联接蛋白hemichannels。205 - 213年,2003年版权2003年Wiley-Liss公司。

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