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Na(+)/Ca(2+) exchanger 2 is neuroprotective by exporting Ca(2+) during a transient focal cerebral ischemia in the mouse

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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.accessioned2010-07-01T07:17:14Z-
dc.date.available2010-07-01T07:17:14Z-
dc.date.issued2008-
dc.identifier.citationCell Calcium. 43 (2008) 482-491en
dc.identifier.issn0143-4160 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17884163-
dc.identifier.urihttp://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6WCC-4PPFTBF-1-F&_cdi=6735&_user=168665&_orig=search&_coverDate=05%2F31%2F2008&_sk=999569994&view=c&wchp=dGLbVlW-zSkWb&md5=50914fe03e5572d1163b720670049456&ie=/sdarticle.pdf-
dc.identifier.urihttps://hdl.handle.net/10371/68170-
dc.description.abstractNa(+)/Ca(2+) exchanger (NCX), by mediating Na(+) and Ca(2+) fluxes bi-directionally, assumes a role in controlling the Ca(2+) 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 Ca(2+) ([Ca(2+)](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 [Ca(2+)](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 Ca(2+) in ischemia and thus protects neuronal cells from death by reducing [Ca(2+)](i) in the adult mouse brain.en
dc.description.sponsorshipThis work was supported by the National Honor Scientist
program of Korea and grants from Korea Institute of Science
and Technology, and the National Creative Research
Initiatives of the Ministry of Science and Technology of
Korea.
en
dc.language.isoenen
dc.publisherElsevieren
dc.subjectAnimalsen
dc.subjectBiological Transporten
dc.subjectBrain/physiopathologyen
dc.subjectCalcium/*metabolismen
dc.subjectCell Survivalen
dc.subjectCerebral Infarction/pathologyen
dc.subjectIschemic Attack, Transient/*metabolism/pathology/physiopathologyen
dc.subjectMembrane Potentialsen
dc.subjectMiceen
dc.subjectMice, Knockouten
dc.subjectNeurons/pathologyen
dc.subjectNeuroprotective Agents/metabolismen
dc.subjectPatch-Clamp Techniquesen
dc.subjectSodium-Calcium Exchanger/genetics/metabolism/*physiologyen
dc.titleNa(+)/Ca(2+) exchanger 2 is neuroprotective by exporting Ca(2+) during a transient focal cerebral ischemia in the mouseen
dc.typeArticleen
dc.contributor.AlternativeAuthor전대종-
dc.contributor.AlternativeAuthor주건-
dc.contributor.AlternativeAuthor정근화-
dc.contributor.AlternativeAuthor김만호-
dc.contributor.AlternativeAuthor윤병우-
dc.contributor.AlternativeAuthor오우택-
dc.contributor.AlternativeAuthor신희섭-
dc.identifier.doi10.1016/j.ceca.2007.08.003-
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