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首页> 外文期刊>Brain research >Involvement of mitochondrial Na(+)-Ca(2+) exchange in intracellular Ca(2+) increase induced by ATP in PC12 cells.
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Involvement of mitochondrial Na(+)-Ca(2+) exchange in intracellular Ca(2+) increase induced by ATP in PC12 cells.

机译：线粒体Na（+）-Ca（2+）交换参与PC12细胞中ATP诱导的细胞内Ca（2+）增加。

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The involvement of mitochondrial Na(+)-Ca(2+) exchange in Ca(2+) responses to ATP was examined in rat pheochromocytoma (PC) 12 cells. Intracellular Ca(2+) ([Ca(2+)](i)) and Na(+) concentrations ([Na(+)](i)) were measured using fura-2 and SBFI, respectively. ATP caused concentration-dependent increases in [Ca(2+)](i) and [Na(+)](i). High concentrations of ATP elicited a Ca(2+) transient followed by a slow recovery of [Ca(2+)](i) (a sustained phase) in 77% of PC12 cells. The sustained phase of Ca(2+) response appeared only when the peak Ca(2+) transient exceeded 500 nM. FCCP, a protonophore, greatly enhanced Ca(2+) responses to ATP only in cells with the sustained phase but not without this phase. The sustained phase was decreased by clonazepam and CGP37157, mitochondrial Na(+)-Ca(2+) exchange inhibitors, and extracellular Na(+) removal but not by cyclosporin A, an inhibitor of permeability transition pores. The reintroduction of Na(+) 3.5 min after ATP stimulation in the absence of Na(+) caused Na(+) concentration-dependent increases in [Ca(2+)](i) and [Na(+)](i). The increase in [Na(+)](i) was correlated with that in [Ca(2+)](i). FCCP caused a great increase in [Ca(2+)](i) 4.5 min after ATP stimulation in the absence of extracellular Na(+) but not in its presence, indicating that mitochondria retain Ca(2+) in the absence of Na(+). These results suggest that ATP causes a large increase in [Ca(2+)](i) which was sequestered in mitochondria and that the sustained phase of Ca(2+) response to ATP are mainly due to the release of mitochondrial Ca(2+) through Na(+)-Ca(2+) exchangers in PC12 cells.
机译：在大鼠嗜铬细胞瘤（PC）12细胞中检查了线粒体Na（+）-Ca（2+）交换中Ca（2+）对ATP的反应。分别使用fura-2和SBFI测量了细胞内Ca（2+）（[Ca（2 +）]（i））和Na（+）浓度（[Na（+）]（i））。 ATP引起[Ca（2 +）]（i）和[Na（+）]（i）中浓度依赖性的增加。高浓度的ATP引起Ca（2+）瞬态，然后在77％的PC12细胞中缓慢恢复[Ca（2 +）]（i）（持续期）。 Ca（2+）响应的持续阶段仅当峰值Ca（2+）瞬态超过500 nM时出现。 FCCP，一个质子体，大大增强了Ca（2+）对ATP的响应，仅在具有持续期的细胞中存在，而没有没有此阶段的细胞。氯硝西am和CGP37157，线粒体Na（+）-Ca（2+）交换抑制剂和细胞外Na（+）去除可降低持续相，但环孢菌素A（通透性过渡孔抑制剂）则不会。在缺少Na（+）的ATP刺激后3.5分钟重新引入Na（+）会导致Na（+）浓度依赖性地增加[Ca（2 +）]（i）和[Na（+）]（i） 。 [Na（+）]（i）的增加与[Ca（2 +）]（i）的增加相关。在没有细胞外Na（+）的情况下，ATP刺激后4.5分钟，FCCP引起[Ca（2 +）]（i）的极大增加，但是在没有细胞外Na（+）的情况下，表明线粒体在没有Na的情况下保留Ca（2+） （+）。这些结果表明，ATP导致线粒体中螯合的[Ca（2 +）]（i）大量增加，并且Ca（2+）对ATP的持续响应主要是由于线粒体Ca（2）的释放+）通过PC12细胞中的Na（+）-Ca（2+）交换剂。

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