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Functional and molecular expression of epithelial sodium channels in cultured human endolymphatic sac epithelial cells.

DC FieldValueLanguage
dc.contributor.author김성헌-
dc.contributor.author최재영-
dc.date.accessioned2015-04-24T17:06:07Z-
dc.date.available2015-04-24T17:06:07Z-
dc.date.issued2009-
dc.identifier.issn1531-7129-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/104763-
dc.description.abstractHYPOTHESIS: Epithelial sodium channels are expressed in cultured human endolymphatic sac (ES) epithelial (HESE) cells and epithelial sodium channel (ENaC) expression is suppressed by interleukin 1beta. BACKGROUND: The ES is part of the membranous labyrinth in the inner ear that plays an important role in maintaining homeostasis of the endolymphatic fluid system. However, the exact mechanism of fluid volume regulation is not yet known. METHODS: The ES specimens were harvested during acoustic neuroma surgery (n = 13) using the translabyrinthine approach and were subcultured with high-epidermal growth factor (25 ng/mL) media. RESULTS: The serially passaged HESE cells differentiated into a monolayer of confluent cells and some of the cultured cells had features of mitochondria-rich cells. Reverse transcription-polymerase chain reaction revealed that ENaC subunits are expressed in the cultured HESE cells. We also confirmed the presence of an ENaC-dependent short-circuit current in the cultured HESE cells. Interestingly, ENaC mRNA expression and ENaC-dependent current decreased after treatment with interleukin 1beta (10 nmol/L for 24 h). CONCLUSION: These findings suggest that ENaC plays an important role in fluid absorption in the human ES and that its function may be altered during inflammatory conditions.-
dc.description.statementOfResponsibilityopen-
dc.format.extent529~534-
dc.relation.isPartOfOTOLOGY & NEUROTOLOGY-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHCell Culture Techniques-
dc.subject.MESHCell Differentiation-
dc.subject.MESHEndolymphatic Sac*/cytology-
dc.subject.MESHEndolymphatic Sac*/physiology-
dc.subject.MESHEpithelial Cells/cytology-
dc.subject.MESHEpithelial Cells/metabolism*-
dc.subject.MESHEpithelial Sodium Channels/biosynthesis*-
dc.subject.MESHGene Expression/drug effects-
dc.subject.MESHHumans-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHInterleukin-1beta/administration & dosage-
dc.subject.MESHMembrane Potentials/drug effects-
dc.subject.MESHMitochondria/metabolism-
dc.subject.MESHProtein Isoforms/biosynthesis-
dc.subject.MESHRNA, Messenger/analysis-
dc.subject.MESHRNA, Messenger/biosynthesis-
dc.subject.MESHRNA, Messenger/genetics-
dc.subject.MESHReverse Transcriptase Polymerase Chain Reaction-
dc.subject.MESHRibosomes/metabolism-
dc.titleFunctional and molecular expression of epithelial sodium channels in cultured human endolymphatic sac epithelial cells.-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Otorhinolaryngology (이비인후과학)-
dc.contributor.googleauthorSung Huhn Kim-
dc.contributor.googleauthorHun Yi Park-
dc.contributor.googleauthorHyun Seung Choi-
dc.contributor.googleauthorHyun Pil Chung-
dc.contributor.googleauthorJae Young Choi-
dc.identifier.doi10.1097/MAO.0b013e31819a8e0e-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA04173-
dc.contributor.localIdA00589-
dc.relation.journalcodeJ02454-
dc.identifier.eissn1537-4505-
dc.identifier.pmid19300301-
dc.identifier.urlhttp://ovidsp.ovid.com/ovidweb.cgi?T=JS&CSC=Y&NEWS=N&PAGE=fulltext&AN=00129492-200906000-00017&LSLINK=80&D=ovft-
dc.contributor.alternativeNameKim, Sung Huhn-
dc.contributor.alternativeNameChoi, Jae Young-
dc.contributor.affiliatedAuthorChoi, Jae Young-
dc.contributor.affiliatedAuthorKim, Sung Huhn-
dc.citation.volume30-
dc.citation.number4-
dc.citation.startPage529-
dc.citation.endPage534-
dc.identifier.bibliographicCitationOTOLOGY & NEUROTOLOGY, Vol.30(4) : 529-534, 2009-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Otorhinolaryngology (이비인후과학교실) > 1. Journal Papers

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