Literature DB >> 22349526

Volume-activated chloride currents in fetal human nasopharyngeal epithelial cells.

Xuerong Sun1, Lixin Chen, Haibing Luo, Jianwen Mao, Linyan Zhu, Sihuai Nie, Liwei Wang.   

Abstract

Volume-activated chloride channels have been studied by us extensively in human nasopharyngeal carcinoma cells. However, the chloride channels in the counterpart of the carcinoma cells have not been investigated. In this study, volume-activated chloride currents (I(cl,vol)) were characterized in normal fetal human nasopharyngeal epithelial cells using the whole-cell patch-clamp technique. Under isotonic conditions, nasopharyngeal epithelial cells displayed only a weak background current. Exposure to 47% hypotonic solution activated a volume-sensitive current. The reversal potential of the current was close to the calculated equilibrium potential for Cl(-). The peak values of the hypotonicity-activated current at +80 mV ranged from 0.82 to 2.71 nA in 23 cells. Further analysis indicated that the density of the hypotonicity-activated current in most cells (18/23) was smaller than 60 pA/pF. Only five cells presented a current larger than 60 pA/pF. The hypotonicity-activated current was independent of the exogenous ATP. Chloride channel inhibitors ATP, tamoxifen and 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), inhibited the current dramatically. The anion permeability of the hypotonicity-activated chloride channels was I(-) > Br(-) > Cl(-) > gluconate. Unexpectedly, in isotonic conditions, ATP (10 mM) activated an inward-rectified current, which had not been observed in the nasopharyngeal carcinoma cells. These results suggest that, under hypotonic challenges, fetal human nasopharyngeal epithelial cells can produce I(cl,vol), which might be involved in cell volume regulation. © Springer Science+Business Media, LLC 2012

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Year:  2012        PMID: 22349526     DOI: 10.1007/s00232-012-9419-5

Source DB:  PubMed          Journal:  J Membr Biol        ISSN: 0022-2631            Impact factor:   1.843


  31 in total

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7.  ClC-3 is a main component of background chloride channels activated under isotonic conditions by autocrine ATP in nasopharyngeal carcinoma cells.

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Journal:  J Cell Physiol       Date:  2011-10       Impact factor: 6.384

8.  Roles of volume-activated Cl- currents and regulatory volume decrease in the cell cycle and proliferation in nasopharyngeal carcinoma cells.

Authors:  L X Chen; L Y Zhu; T J C Jacob; L W Wang
Journal:  Cell Prolif       Date:  2007-04       Impact factor: 6.831

9.  Blockage of volume-activated chloride channels inhibits migration of nasopharyngeal carcinoma cells.

Authors:  Jianwen Mao; Liwei Wang; Aihui Fan; Jianhong Wang; Bin Xu; Tim J C Jacob; Lixin Chen
Journal:  Cell Physiol Biochem       Date:  2007

10.  Volume-sensitive outwardly rectifying chloride channel in white adipocytes from normal and diabetic mice.

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Journal:  Am J Physiol Cell Physiol       Date:  2010-01-27       Impact factor: 4.249

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Review 3.  Cystic fibrosis transmembrane conductance regulator-emerging regulator of cancer.

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4.  High glucose inhibits ClC-2 chloride channels and attenuates cell migration of rat keratinocytes.

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Journal:  Drug Des Devel Ther       Date:  2015-08-28       Impact factor: 4.162

5.  Functional expression of chloride channels and their roles in the cell cycle and cell proliferation in highly differentiated nasopharyngeal carcinoma cells.

Authors:  Weiyuan Huang; Mei Liu; Linyan Zhu; Shanwen Liu; Hai Luo; Lianshun Ma; Haibo Wang; Ruiling Lu; Xiaoxue Sun; Lixin Chen; Liwei Wang
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  5 in total

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