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ClC-3氯通道对Thapsigargin触发的Ca2＋运动的影响 被引量：2

Effects of ClC-3 chloride channel on the Ca^(2+) movement induced by Thapsigargin in PC12 cells
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摘要 目的探讨ClC-3氯通道与Thapsigargin(TG)触发的Ca2+运动的关系。方法在PC12细胞中转染全长ClC-3cDNA,利用生物荧光影像分析系统测定胞质Ca2+技术探讨ClC-3氯通道对TG触发的Ca2+运动的影响。结果与对照组相比,ClC-3蛋白过表达对TG触发的PC12细胞静息[Ca2+]i的Ratio值和Ca2+释放的Ratio值无影响(P>0.05)。但使Ca2+内流量明显降低(P<0.05)。SK&F96365可以浓度依赖的抑制TG触发的Ca2+内流,但与对照细胞及空载体转染细胞相比,SK&F96365对ClC-3蛋白过表达细胞Ca2+内流的抑制作用明显减弱(P<0.05)。结论ClC-3蛋白参与TG触发的经Ca2+池操纵的Ca2+内流(store-operated Ca2+entry,SOCE)调节。 Aim To investigate the relationship be- tween C1C-3 chloride channels and Ca2＋ movement in- duced by thapsigargin （TG） in PC12 cells. Methods The concentration of intracellular free calcium （ [ Ca2＋ ] i ） expressed as the ratio value （ Intensity340/ Intensity380） was determined with Fura-2/AM probe. Results The overexpression of ClC-3 protein caused a significant decrease in TG-induced Ca2＋ influx com- pared with control cells, and cells transfected with pcD- NA3. 1,whereas the [ Ca2＋ ]i at resting level and at peak level was not different among all groups （P 〉O. 05 ）. SK ＆ F96365 at the concentration of 5 -20 μmol · L-1 inhibited the Ca2＋ influx induced by 1.0 μmol · L-1 Thapsigargin in a concentration-dependent manner. The inhibitory effect of SK ＆ F96365 on Ca2＋ influx was decreased by overexpression of ClC-3 pro- tein. Conclusion ClC-3 chloride channel was involved in the regulation of store-operated Ca2＋ entry （SOCE）.
作者 张海宁 丘钦英 关永源
机构地区 中山大学中山医学院药理学教研室
出处 《中国药理学通报》 CAS CSCD 北大核心 2008年第8期1057-1061,共5页 Chinese Pharmacological Bulletin
基金 国家自然科学基金资助项目(No30271503) 中华医学会基金资助项目(CMB,No00730) 国家教育部博士点基金资助项目(No20020558055) 广东省自然科学基金团队项目资助项目
关键词 ClC-3氯通道 过表达 钙离子 THAPSIGARGIN ClC-3 chloride channel overexpression Ca2＋ Thapsigargin
分类号 R329.2 [医药卫生—人体解剖和组织胚胎学] R329.25 [医药卫生—人体解剖和组织胚胎学]
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参考文献17

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中国药理学通报
2008年 第8期

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