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ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells.
Am J Physiol Cell Physiol 2012; 303(1):C14-23AJ

Abstract

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.

Authors+Show Affiliations

Department of Physiology, Medical College, Jinan University, Guangzhou, China. wangliweic@sohu.comNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

22496242

Citation

Wang, Liwei, et al. "ClC-3 Is a Candidate of the Channel Proteins Mediating Acid-activated Chloride Currents in Nasopharyngeal Carcinoma Cells." American Journal of Physiology. Cell Physiology, vol. 303, no. 1, 2012, pp. C14-23.
Wang L, Ma W, Zhu L, et al. ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells. Am J Physiol, Cell Physiol. 2012;303(1):C14-23.
Wang, L., Ma, W., Zhu, L., Ye, D., Li, Y., Liu, S., ... Chen, L. (2012). ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells. American Journal of Physiology. Cell Physiology, 303(1), pp. C14-23. doi:10.1152/ajpcell.00145.2011.
Wang L, et al. ClC-3 Is a Candidate of the Channel Proteins Mediating Acid-activated Chloride Currents in Nasopharyngeal Carcinoma Cells. Am J Physiol, Cell Physiol. 2012 Jul 1;303(1):C14-23. PubMed PMID: 22496242.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - ClC-3 is a candidate of the channel proteins mediating acid-activated chloride currents in nasopharyngeal carcinoma cells. AU - Wang,Liwei, AU - Ma,Wenbo, AU - Zhu,Linyan, AU - Ye,Dong, AU - Li,Yuan, AU - Liu,Shanwen, AU - Li,Huarong, AU - Zuo,Wanhong, AU - Li,Bingxue, AU - Ye,Wencai, AU - Chen,Lixin, Y1 - 2012/04/11/ PY - 2012/4/13/entrez PY - 2012/4/13/pubmed PY - 2012/9/12/medline SP - C14 EP - 23 JF - American journal of physiology. Cell physiology JO - Am. J. Physiol., Cell Physiol. VL - 303 IS - 1 N2 - 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. SN - 1522-1563 UR - https://www.unboundmedicine.com/medline/citation/22496242/ClC_3_is_a_candidate_of_the_channel_proteins_mediating_acid_activated_chloride_currents_in_nasopharyngeal_carcinoma_cells_ L2 - http://www.physiology.org/doi/full/10.1152/ajpcell.00145.2011?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -