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The acetylation of p53 is regulated by Class I <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>s and, because p53 appears to play a role in ischemic pathology, the purpose of this study was to discover, using an <jats:italic>in vitro<\/jats:italic> white matter ischemia model and an <jats:italic>in vivo<\/jats:italic> cerebral ischemia model, if neuroprotection mediated by <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content> inhibition depended on p53 expression. Optic nerves were excised from wild\u2010type and p53\u2010deficient mice, and then subjected to oxygen\u2013glucose deprivation in the presence and absence of a specific inhibitor of Class I <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content>s (<jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>\u2010275, entinostat) while compound action potentials were recorded. Furthermore, transient focal ischemia was imposed on wild\u2010type and p53\u2010deficient mice, which were subsequently treated with <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>\u2010275. Interestingly, and in both scenarios, the beneficial effects of <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>\u2010275 were most pronounced when p53 was absent. These results suggest that modulation of p53 activity is not responsible for <jats:styled-content style=\"fixed-case\">MS<\/jats:styled-content>\u2010275\u2010mediated neuroprotection, and further illustrate how <jats:styled-content style=\"fixed-case\">HDAC<\/jats:styled-content> inhibitors variably influence p53 and associated apoptotic pathways.\n<jats:boxed-text content-type=\"graphic\" position=\"anchor\"><jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc12498-fig-0008-m.png\"><jats:alt-text>image<\/jats:alt-text><\/jats:graphic><\/jats:boxed-text>\nOptic nerves from wild\u2010type and p53\u2010deficient mice, engineered to express cyan fluorescent protein (CFP) in neuronal mitochondria, were subjected to oxygen\u2013glucose deprivation (OGD) in the presence and absence of a specific inhibitor of Class I histone deacetylases. The protective effect of MS\u2010275 was evidenced by mitochondrial preservation, and this was most pronounced in the absence of p53.<\/jats:p>","DOI":"10.1111\/jnc.12498","type":"journal-article","created":{"date-parts":[[2013,10,21]],"date-time":"2013-10-21T19:14:55Z","timestamp":1382382895000},"page":"509-515","source":"Crossref","is-referenced-by-count":33,"title":["<scp>MS<\/scp>\u2010275, a Class I histone deacetylase inhibitor, protects the p53\u2010deficient mouse against ischemic injury"],"prefix":"10.1111","volume":"129","author":[{"given":"Sean P.","family":"Murphy","sequence":"first","affiliation":[{"name":"Department of Neurological Surgery University of Washington School of Medicine Seattle Washington USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rona J.","family":"Lee","sequence":"additional","affiliation":[{"name":"Department of Neurological Surgery University of Washington School of Medicine Seattle Washington 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