{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T17:46:49Z","timestamp":1778694409302,"version":"3.51.4"},"reference-count":43,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2012,8,20]],"date-time":"2012-08-20T00:00:00Z","timestamp":1345420800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Glia"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The Bcl\u20102\u2010interacting death suppressor (Bis) protein is involved in antiapoptosis and antistress pathways. However, its roles after neonatal hypoxia\u2013ischemia remain obscure. Therefore, we investigated the effects of Bis deletion on hippocampal cell death following neonatal hypoxia\u2013ischemia. We transected the right common carotid artery of <jats:italic>bis<\/jats:italic><jats:sup>+\/+<\/jats:sup> and <jats:italic>bis<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice at postnatal Day 7 and subjected them to hypoxia for 35 min. Cresyl violet staining showed that hypoxia\u2013ischemia induced progressive cell death in the hippocampi of <jats:italic>bis<\/jats:italic><jats:sup>+\/+<\/jats:sup> mice. Moreover, Bis was expressed in astrocytes, not microglia, in sham\u2010manipulated hippocampi of <jats:italic>bis<\/jats:italic><jats:sup>+\/+<\/jats:sup> mice, and was markedly enhanced after hypoxia\u2013ischemia. Immunoblotting showed that Bis expression significantly increased 3 and 7 days following hypoxia\u2013ischemia. Unexpectedly, 7 days after hypoxia\u2013ischemia, the number of hippocampal NeuN\u2010positive cells was higher in the <jats:italic>bis<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice than in the <jats:italic>bis<\/jats:italic><jats:sup>+\/+<\/jats:sup> mice. We subsequently performed transcriptomic analysis and quantitative real time polymerase chain reaction to search for the underlying genes responsible for resistance to hypoxia\u2013ischemia in the <jats:italic>bis<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> hippocampus. These studies showed that 6 h after hypoxia\u2013ischemia, galectin 3 and filamin C levels increased to a lesser extent in the <jats:italic>bis<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> hippocampi compared with the <jats:italic>bis<\/jats:italic><jats:sup>+\/+<\/jats:sup> hippocampi. Finally, our <jats:italic>in vitro<\/jats:italic> hypoxia\u2013ischemia model, using A172 glioma cells and primary astrocytes, showed that downregulation of Bis blocked the enhanced expression of galectin 3 after oxygen\u2013glucose deprivation. This study demonstrated that Bis was upregulated in the astrocytes after hypoxia\u2013ischemia. In addition, we showed that hippocampal neurons are less vulnerable to hypoxia\u2013ischemia in mice lacking Bis, possibly because of the modulation of galectin 3 induction. \u00a9 2012 Wiley Periodicals, Inc.<\/jats:p>","DOI":"10.1002\/glia.22407","type":"journal-article","created":{"date-parts":[[2012,8,20]],"date-time":"2012-08-20T14:17:27Z","timestamp":1345472247000},"page":"1915-1929","source":"Crossref","is-referenced-by-count":10,"title":["Decreased vulnerability of hippocampal neurons after neonatal hypoxia\u2013ischemia in <i>bis<\/i>\u2010deficient 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