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dc.contributor.authorJeon, Daejong-
dc.contributor.authorChu, Kon-
dc.contributor.authorJung, Keun-Hwa-
dc.contributor.authorKim, Manho-
dc.contributor.authorYoon, Byung-Woo-
dc.contributor.authorLee, C. Justin-
dc.contributor.authorOh, Uhtaek-
dc.contributor.authorShin, Hee-Sup-
dc.date.accessioned2024-01-20T23:30:52Z-
dc.date.available2024-01-20T23:30:52Z-
dc.date.created2021-09-03-
dc.date.issued2008-05-
dc.identifier.issn0143-4160-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/133519-
dc.description.abstractNa+/Ca2+ exchanger (NCX), by mediating Na+ and Ca2+, fluxes bi-directionally, assumes a role in controlling the Ca2+ homeostasis in the ischemic brain. It has been suggested that the three isoforms of NCX (NCX1, 2 and 3) may be differentially involved in permanent cerebral ischemia. However, the role of NCX2 has not been defined in ischemic reperfusion injury after a transient focal cerebral ischemia. Furthermore, it is not known whether NCX2 imports or exports intracellular Ca2+([Ca2+](i)) following ischemia and reperfusion. To define the role of NCX2 in ischemia and reperfusion, we examined mice lacking NCX2, in vivo and in vitro. After an in vitro ischemia, a significantly slower recovery in population spike amplitudes, a sustained elevation of [Ca2+](i) and an increased membrane depolarization were developed in the NCX2-deficient hippocampus. Moreover, a transient focal cerebral ischemia in vivo produced a larger infarction and more cell death in the NCX2-deficient mouse brain. In particular, in the wild type brain, NCX2-expressing neurons were largely spared from cell death after ischemia. Our results suggest that NCX2 exports Ca2+ in ischemia and thus protects neuronal cells from death by reducing [Ca2+](i) in the adult mouse brain. (c) 2007 Elsevier Ltd. All rights reserved.-
dc.languageEnglish-
dc.publisherELSEVIER SCI LTD-
dc.subjectSODIUM-CALCIUM EXCHANGE-
dc.subjectNA+-CA2+ EXCHANGER-
dc.subjectBRAIN-REGIONS-
dc.subjectRAT-BRAIN-
dc.subjectIN-VITRO-
dc.subjectEXPRESSION-
dc.subjectNCX3-
dc.subjectISOFORMS-
dc.subjectNEURONS-
dc.subjectCLONING-
dc.titleNa+/Ca2+ exchanger 2 is neuroprotective by exporting Ca2+ during a transient focal cerebral ischemia in the mouse-
dc.typeArticle-
dc.identifier.doi10.1016/j.ceca.2007.08.003-
dc.description.journalClass1-
dc.identifier.bibliographicCitationCELL CALCIUM, v.43, no.5, pp.482 - 491-
dc.citation.titleCELL CALCIUM-
dc.citation.volume43-
dc.citation.number5-
dc.citation.startPage482-
dc.citation.endPage491-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000256325900006-
dc.identifier.scopusid2-s2.0-42149087628-
dc.relation.journalWebOfScienceCategoryCell Biology-
dc.relation.journalResearchAreaCell Biology-
dc.type.docTypeArticle-
dc.subject.keywordPlusSODIUM-CALCIUM EXCHANGE-
dc.subject.keywordPlusNA+-CA2+ EXCHANGER-
dc.subject.keywordPlusBRAIN-REGIONS-
dc.subject.keywordPlusRAT-BRAIN-
dc.subject.keywordPlusIN-VITRO-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusNCX3-
dc.subject.keywordPlusISOFORMS-
dc.subject.keywordPlusNEURONS-
dc.subject.keywordPlusCLONING-
dc.subject.keywordAuthorcerebral ischemia-
dc.subject.keywordAuthorNa+/Ca2+ exchanger-
dc.subject.keywordAuthorNCX2-deficient mice-
dc.subject.keywordAuthor[Ca2+](i)-
dc.subject.keywordAuthorpopulation spike-
dc.subject.keywordAuthormembrane depolarization-
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