Modifications of Ca2+ mobilization and noradrenaline release by S-nitroso-cysteine in PC12 cells.
Modifications of Ca2+ mobilization and noradrenaline release by S-nitroso-cysteine in PC12 cells.
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PC12 细胞中 S-亚硝基-半胱氨酸对 Ca2 动员和去甲肾上腺素释放的修饰。
DOI：
10.1006/abbi.1999.1075
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发表时间：
1999
影响因子：
3.9
通讯作者：
Y. Nomura
中科院分区：
文献类型：
--
作者：
T. Naganuma;T. Murayama;Y. Nomura
研究了一氧化氮（NO）相关化合物对神经分泌型PC 12细胞胞浆游离Ca ~（2+）浓度（[Ca ~（2+）]i）和去甲肾上腺素（NA）释放的影响。加入S-亚硝基半胱氨酸（SNC）刺激胞内[Ca ~（2+）]i以浓度依赖性方式持续增加。其他NO供体，刺激环GMP积累，没有引起[Ca 2 +]i增加。用0.2 mM SNC处理后，咖啡因诱导的[Ca 2 +]i从Ca 2+池的瞬时增加被完全消除。N-乙基马来酰亚胺（NEM）的加入引起细胞内Ca 2+池的[Ca 2 +]i持续增加。此外，咖啡因并没有刺激进一步的[Ca 2 +]i增加与NEM预处理的PC 12细胞。这些发现表明，SNC和NEM主要与咖啡因敏感的Ca 2+池相互作用。添加二硫苏糖醇（DTT）到0.4 mM SNC刺激的细胞降低[Ca 2 +]i到基础水平，并添加DTT到NEM刺激的细胞锁定[Ca 2 +]i在高水平。DTT预处理不能消除SNC而非NEM的刺激作用。这些研究结果表明，SNC或NEM的咖啡因敏感性受体上的巯基的氧化状态的修改调节Ca 2+通道活性以可逆的方式。SNC本身不刺激NA释放，但抑制离子霉素刺激的NA释放。与此相反，NEM刺激NA释放细胞外CaCl 2的情况下，进一步增强离子霉素刺激NA释放。SNC从咖啡因敏感池中动员Ca 2+并不是一个充分的因素，刺激NA释放的其他因素可能受到SNC的负调节。
The effects of nitrogen monoxide (NO)-related compounds on cytosolic free Ca2+ concentrations ([Ca2+]i) and noradrenaline (NA) release in neurosecretory PC12 cells were investigated. The addition of S-nitroso-cysteine (SNC) stimulated [Ca2+]i increases from an intracellular Ca2+ pool continuously in a concentration-dependent manner. Other NO donors, which stimulate cyclic GMP accumulation, did not cause [Ca2+]i increases. After treatment with 0.2 mM SNC, transient increases in [Ca2+]i from the Ca2+ pool induced by caffeine were completely abolished. The addition of N-ethylmaleimide (NEM) caused sustained [Ca2+]i increases from the intracellular Ca2+ pool. Furthermore, caffeine did not stimulate further [Ca2+]i increases in PC12 cells pretreated with NEM. These findings suggest that SNC and NEM predominantly interact with a caffeine-sensitive Ca2+ pool. The addition of dithiothreitol (DTT) to 0.4 mM SNC-stimulated cells reduced [Ca2+]i to basal levels, and the addition of DTT to NEM-stimulated cells locked [Ca2+]i at high levels. The stimulatory effects of SNC but not NEM were not abolished by pretreatment with DTT. These findings suggest that modification of the oxidation status of the sulfhydryl groups on the caffeine-sensitive receptors by SNC or NEM regulates Ca2+ channel activity in a reversible manner. SNC did not stimulate NA release by itself but did inhibit ionomycin-stimulated NA release. In contrast, NEM stimulated NA release in the absence of extracellular CaCl2 and further enhanced ionomycin-stimulated NA release. Ca2+ mobilization by SNC from the caffeine-sensitive pool was not a sufficient factor, and other factors stimulating NA release may be negatively regulated by SNC.
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