Targeted disruption of the bcl-2 gene in mice exacerbates focal ischemic brain injury

dc.contributor.authorHata, R.en
dc.contributor.authorGillardon, F.en
dc.contributor.authorMichaelidis, T. M.en
dc.contributor.authorHossmann, K. A.en
dc.date.accessioned2015-11-24T16:32:09Z
dc.date.available2015-11-24T16:32:09Z
dc.identifier.issn0885-7490-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/7522
dc.rightsDefault Licence-
dc.subjectcerebral ischemiaen
dc.subjectfocal ischemiaen
dc.subjectmutant miceen
dc.subjectbcl-2en
dc.subjectapoptosisen
dc.subjectcerebral-artery occlusionen
dc.subjectcell-deathen
dc.subjectendoplasmic-reticulumen
dc.subjectglobal-ischemiaen
dc.subjecttransgenic miceen
dc.subjectcytochrome-cen
dc.subjectapoptosisen
dc.subjectneuronsen
dc.subjectbaxen
dc.subjectexpressionen
dc.titleTargeted disruption of the bcl-2 gene in mice exacerbates focal ischemic brain injuryen
heal.abstractNeuronal death after brain ischemia is mainly due to necrosis but there is also evidence for involvement of apoptosis. To test the importance of apoptosis, we investigated the effect of targeted disruption of the apoptosis-suppressive gene bcl-2 on the severity of ischemic brain injury. Transient focal ischemia for 1 hour was induced by occlusion of the middle cerebral artery in homozygous (n = 7) and heterozygous (n = 6) bcl-2 knockout mice as well as in their wildtype littermates (n = 5). Bcl-2 ablation did not influence cerebral blood flow but it significantly increased infarct size and neurological deficit score at 1 day after reperfusion in a gene-dose dependent manner. The exacerbation of tissue damage in the absence of Bcl-2 underscores the importance of apoptotic pathways for the manifestation of ischemic injury after transient vascular occlusion.en
heal.accesscampus-
heal.fullTextAvailabilityTRUE-
heal.identifier.secondary<Go to ISI>://000082385100005-
heal.journalNameMetabolic Brain Diseaseen
heal.journalTypepeer reviewed-
heal.languageen-
heal.publicationDate1999-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών και Τεχνολογιών. Τμήμα Βιολογικών Εφαρμογών και Τεχνολογιώνel
heal.typejournalArticle-
heal.type.elΆρθρο Περιοδικούel
heal.type.enJournal articleen

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