ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells
ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells
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ClC-3 是介导鼻咽癌细胞酸激活氯电流的通道蛋白候选者
DOI：
10.1152/ajpcell.00145.2011
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发表时间：
2012-07-01
影响因子：
5.5
通讯作者：
Chen, Lixin
中科院分区：
文献类型：
--
作者：
Wang, Liwei;Ma, Wenbo;Chen, Lixin
王L，马伟，朱L，叶东，李勇，刘S，李H，左伟，李波，叶伟，陈丽丽。ClC-3是介导鼻咽癌细胞酸激活氯电流的候选通道蛋白。Am J Physiol Cell Physiol 303：C14-C23,2012。首次发表于2012年4月11日；doi:10.1152/ajpcell.00145.2011.-Acid-activated氯电流已在几种细胞类型中被报道，并可能在细胞功能调节中发挥重要作用。然而，调节电流的通道的分子同一性还没有定义。本文研究了人鼻咽癌细胞(CNE-2Z)酸诱导氯电流的激活以及酸激活氯通道的可能候选者。当细胞外pH从7.4时降至6.6时，氯电流被激活。然而，当细胞外pH进一步降低到5.8时，该电流被抑制。该电流呈微弱的外向整流，可被高张引起的细胞收缩和氯离子通道阻断剂5-硝基-2-3-苯丙氨基苯甲酸(NPPB)、他莫昔芬和4，4‘-二异硫氰基二苯乙烯-2，2’-二磺酸二钠(DIDS)所抑制。通道对阴离子的通透性顺序为：I->；bR->；Cl->；葡萄糖酸(-)。在CLC氯通道中，CLC-3和CLC-7在CNE-2Z细胞中高表达。用ClC-3小干扰(Si)RNA抑制ClC-3的表达可阻止酸诱导电流的激活，但用ClC-7 siRNA抑制ClC-7的表达并不显著影响该电流。结果提示，介导酸性氯离子电流的氯通道具有体积敏感性。ClC-3是介导或调节鼻咽癌细胞酸激活氯电流的候选通道蛋白。
Wang L, Ma W, Zhu L, Ye D, Li Y, Liu S, Li H, Zuo W, Li B, Ye W, Chen L. ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells. Am J Physiol Cell Physiol 303: C14-C23, 2012. First published April 11, 2012; doi:10.1152/ajpcell.00145.2011.-Acid-activated chloride currents have been reported in several cell types and may play important roles in regulation of cell function. However, the molecular identities of the channels that mediate the currents are not defined. In this study, activation of the acid-induced chloride current and the possible candidates of the acid-activated chloride channel were investigated in human nasopharyngeal carcinoma cells (CNE-2Z). A chloride current was activated when extracellular pH was reduced to 6.6 from 7.4. However, a further decrease of extracellular pH to 5.8 inhibited the current. The current was weakly outward-rectified and was suppressed by hypertonicity-induced cell shrinkage and by the chloride channel blockers 5-nitro-2-3-phenylpropylamino benzoic acid (NPPB), tamoxifen, and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid disodium salt hydrate (DIDS). The permeability sequence of the channel to anions was I- > Br- > Cl- > gluconate(-). Among the ClC chloride channels, ClC-3 and ClC-7 were strongly expressed in CNE-2Z cells. Knockdown of ClC-3 expression with ClC-3 small interfering (si) RNA prevented the activation of the acid-induced current, but silence of ClC-7 expression with ClC-7 siRNA did not significantly affect the current. The results suggest that the chloride channel mediating the acid-induced chloride current was volume sensitive. ClC-3 is a candidate of the channel proteins that mediate or regulate the acid-activated chloride current in nasopharyngeal carcinoma cells.