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The Change of Taurine Transport in Variable Stress States through the Inner Blood-Retinal Barrier using In Vitro Model

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dc.contributor.authorKang, Young-Sook-
dc.contributor.authorLee, Na-Young-
dc.contributor.authorChung, Yeon-Yee-
dc.date.available2021-02-22T14:17:29Z-
dc.date.issued2009-04-
dc.identifier.issn1976-9148-
dc.identifier.issn2005-4483-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/13771-
dc.description.abstractTaurine is the most abundant free amino acid in the retina and transported into retina via taurine transporter (TauT) at the inner blood-retinal barrier (iBRB). In the present study, we investigated whether the taurine transport at the iBRB is regulated by oxidative stress or disease-like state in a conditionally immortalized rat retinal capillary endothelial cell line (TR-iBRB) used as an in vitro model of iBRB. First, [H-3]taurine uptake and efflux by TR-iBRB were regulated in the presence of extracellular Ca2+. [H-3]Taurine uptake was inhibited and efflux was enhanced under Ca2+ free condition in the cells. In addition, oxidative stress inducing agents such as tumor necrosis factor-alpha (TNF-alpha), lipopolysaccharide (LPS), diethyl maleate (DEM) and glutamate increased [H-3]taurine uptake and decreased [H-3]taurine efflux in TR-iBRB cells. Whereas, 3-morpholinosydnonimine (SIN-1), which is known to NO donor decreased [H-3]taurine uptake. Lastly, TR-iBRB cells exposed to high glucose (25 mM) medium and the [H-3]taurine uptake was reduced about 20% at the condition. Also, [H-3]taurine uptake was decreased by cytochalasin B, which is known to glucose transport inhibitor. In conclusion, taurine transport in TR-iBRB cells is regulated diversely at extracellular Ca2+, oxidative stress and hyperglycemic condition. It suggested that taurine would play a role as a retinal protector in diverse disease states.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherKOREAN SOC APPLIED PHARMACOLOGY-
dc.titleThe Change of Taurine Transport in Variable Stress States through the Inner Blood-Retinal Barrier using In Vitro Model-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.4062/biomolther.2009.17.2.175-
dc.identifier.scopusid2-s2.0-69549105720-
dc.identifier.wosid000266067200010-
dc.identifier.bibliographicCitationBIOMOLECULES & THERAPEUTICS, v.17, no.2, pp 175 - 180-
dc.citation.titleBIOMOLECULES & THERAPEUTICS-
dc.citation.volume17-
dc.citation.number2-
dc.citation.startPage175-
dc.citation.endPage180-
dc.type.docTypeArticle-
dc.identifier.kciidART001338724-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaPharmacology & Pharmacy-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryPharmacology & Pharmacy-
dc.subject.keywordPlusCARRIER-MEDIATED TRANSPORT-
dc.subject.keywordPlusNECROSIS-FACTOR-ALPHA-
dc.subject.keywordPlusBRAIN-BARRIER-
dc.subject.keywordPlusNITRIC-OXIDE-
dc.subject.keywordPlusAMINO-ACIDS-
dc.subject.keywordPlusCELL-LINES-
dc.subject.keywordPlusRAT-
dc.subject.keywordPlusHYPERTONICITY-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusRESIDUES-
dc.subject.keywordAuthorTaurine transport-
dc.subject.keywordAuthorInner blood-retinal barrier-
dc.subject.keywordAuthorConditionally immortalized rat retinal capillary endothelial cells-
dc.subject.keywordAuthorOxidative stress-
dc.subject.keywordAuthorHyperglycemic condition-
dc.subject.keywordAuthorExtracellular calcium-
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