title: Volume-activated chloride currents in fetal human nasopharyngeal epithelial cells.
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.
authors.affiliation: Institute of Aging Research, Key Laboratory for Medical Molecular Diagnostics of Guangdong Province, Guangdong Medical College, Dongguan 523808, China. xuerongsun@126.com
authors.forename: Xuerong
authors.initials: X
authors.lastname: Sun
authors.forename: Lixin
authors.initials: L
authors.lastname: Chen
authors.forename: Haibing
authors.initials: H
authors.lastname: Luo
authors.forename: Jianwen
authors.initials: J
authors.lastname: Mao
authors.forename: Linyan
authors.initials: L
authors.lastname: Zhu
authors.forename: Sihuai
authors.initials: S
authors.lastname: Nie
authors.forename: Liwei
authors.initials: L
authors.lastname: Wang
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology; D000838:Anions / Q000378:metabolism; D002463:Cell Membrane Permeability / Q000187:drug effects / Q000502:physiology; D048429:Cell Size / Q000187:drug effects; D018118:Chloride Channels / Q000037:antagonists & inhibitors* / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism*; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D006801:Humans; D007038:Hypotonic Solutions; D007552:Isotonic Solutions; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009305:Nasopharynx / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D009579:Nitrobenzoates / Q000494:pharmacology; D013629:Tamoxifen / Q000494:pharmacology
chemical_list: D000838:Anions; D018118:Chloride Channels; D002712:Chlorides; D007038:Hypotonic Solutions; D007552:Isotonic Solutions; D009579:Nitrobenzoates; D013629:Tamoxifen; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D000255:Adenosine Triphosphate