External bioenergy-induced increases in intracellular free calcium concentrations are mediated by Na+/Ca2+ exchanger and L-type calcium channel
External bioenergy-induced increases in intracellular free calcium concentrations are mediated by Na+/Ca2+ exchanger and L-type calcium channel
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外部生物能诱导的细胞内游离钙浓度增加由 Na /Ca2 交换器和 L 型钙通道介导
DOI：
10.1007/s11010-005-3615-x
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发表时间：
2005
影响因子：
4.3
通讯作者：
W. Jonas
中科院分区：
文献类型：
--
作者：
J. Kiang;J. Ives;W. Jonas
体外生物能量(EBE，从人体发出的能量)可增加培养的人淋巴Jurkat T细胞内钙离子浓度([Ca~(2+)]i，这是信号转导中的一个重要因素)，并调节细胞对热应激的反应。在这项研究中，我们想要阐明其潜在的机制。一位生物能源专家在含有不同离子成分或不同浓度抑制剂的缓冲液中，连续向培养的Jurkat T细胞试管发射生物能量，时间为15分钟。用荧光探针Fura-2荧光分光光度法测定[Ca~(2+)]i。Jurkat T细胞静息[Ca2+]i在正常缓冲液中为70±3 nM(n=130)。去除外源性钙离子使静息[Ca~(2+)]_i下降至52±2 nM(n=23)，表明外源性[Ca~(2+)]_i内流对维持[Ca~(2+)]_i的基础水平有重要作用。EBE处理Jurkat T细胞15分钟后，[Ca~(2+)]_i升高30±5%(P<0.05，≤，t检验)。生物能源专家和Jurkat T细胞之间的距离以及EBE的重复治疗并没有减弱[Ca2+]i对EBE的反应。去除外源性钙离子或钠离子而不清除镁离子可抑制EBE引起的细胞内钙离子浓度升高，Na+/Ca~(2+)交换抑制剂二氯苯甲胺也呈浓度依赖性地抑制EBE引起的细胞内钙离子浓度升高，其IC50为0.11±0.02 nM。当外加[K+]由4.5 mM增加到25 mM时，EBE使[Ca~(2+)]i降低，此作用也可被L电压门控型钙通道阻断剂维拉帕米所阻断。这些结果表明，EBE诱导的[Ca~(2+)]i升高可以作为评估和验证生物能源效应和那些声称生物能源能力的专家的客观手段。[Ca~(2+)]i的升高是通过激活Na~+/Ca~(2+)交换器和开放L型电压门控钙通道来实现的。(摩尔细胞生物化学271：51-59,2005)
External bioenergy (EBE, energy emitted from a human body) has been shown to increase intracellular calcium concentration ([Ca2+]i, an important factor in signal transduction) and regulate the cellular response to heat stress in cultured human lymphoid Jurkat T cells. In this study, we wanted to elucidate the underlying mechanisms. A bioenergy specialist emitted bioenergy sequentially toward tubes of cultured Jurkat T cells for one 15-minute period in buffers containing different ion compositions or different concentrations of inhibitors. [Ca2+]i was measured spectrofluorometrically using the fluorescent probe fura-2. The resting [Ca2+]i in Jurkat T cells was 70 ± 3 nM (n = 130) in the normal buffer. Removal of external calcium decreased the resting [Ca2+]i to 52 ± 2 nM (n = 23), indicating that [Ca2+] entry from the external source is important for maintaining the basal level of [Ca2+]i. Treatment of Jurkat T cells with EBE for 15 min increased [Ca2+]i by 30 ± 5% (P ≤ 0.05, Student t-test). The distance between the bioenergy specialist and Jurkat T cells and repetitive treatments of EBE did not attenuate [Ca2+]i responsiveness to EBE. Removal of external Ca2+ or Na+, but not Mg2+, inhibited the EBE-induced increase in [Ca2+]i. Dichlorobenzamil, an inhibitor of Na+/Ca2+ exchangers, also inhibited the EBE-induced increase in [Ca2+]i in a concentration-dependent manner with an IC50 of 0.11 ± 0.02 nM. When external [K+] was increased from 4.5 mM to 25 mM, EBE decreased [Ca2+]i. The EBE-induced increase was also blocked by verapamil, an L-type voltage-gated Ca2+ channel blocker. These results suggest that the EBE-induced [Ca2+]i increase may serve as an objective means for assessing and validating bioenergy effects and those specialists claiming bioenergy capability. The increase in [Ca2+]i is mediated by activation of Na+/Ca2+ exchangers and opening of L-type voltage-gated Ca2+ channels. (Mol Cell Biochem 271: 51–59, 2005)
阿片类药物通过 δ 受体作用，引起背根神经节-神经母细胞瘤杂交 ND8-47 细胞细胞内游离钙浓度的短暂增加。
DOI：
--
发表时间：
1994
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Tang,T;Kiang,JG;Cox,BM
通讯作者：
Cox,BM
大鼠对吗啡心动过缓的耐受性。
DOI：
--
发表时间：
1983
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Kiang,JG;Dewey,WL;Wei,ET
通讯作者：
Wei,ET