{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T05:38:42Z","timestamp":1774330722280,"version":"3.50.1"},"reference-count":54,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2021,9,6]],"date-time":"2021-09-06T00:00:00Z","timestamp":1630886400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R35NS097299"],"award-info":[{"award-number":["R35NS097299"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["R56NS114563"],"award-info":[{"award-number":["R56NS114563"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004543","name":"China Scholarship Council","doi-asserted-by":"publisher","award":["201806230241"],"award-info":[{"award-number":["201806230241"]}],"id":[{"id":"10.13039\/501100004543","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The cellular responses to hypoxia or hypoxia\u2010ischemia (HI) are governed largely by the hypoxia\u2010inducible factor (HIF) family of transcription factors. Our previous studies show that HIF\u20101\u03b1 induction is an important factor that mediates protective effects in the brain after neonatal HI. In the present study, we investigated the contribution of another closely related HIF \u03b1 isoform, HIF\u20102\u03b1, specifically the neuronal HIF\u20102\u03b1, to brain HI injury. Homozygous transgenic mice with a floxed exon 2 of HIF\u20102\u03b1 were bred with CaMKII\u03b1\u2010Cre mice to generate a mouse line with selective deletion of HIF\u20102\u03b1 in forebrain neurons. These mice, along with their wildtype littermates, were subjected to HI at postnatal day 9. Brain injury at different ages was evaluated by the levels of cleaved caspase\u20103 and spectrin breakdown products at 24\u00a0hr; and histologically at 6\u00a0days or 3\u00a0months after HI. Multiple behavioral tests were performed at 3\u00a0months, prior to sacrifice. Loss of neuronal HIF\u20102\u03b1 exacerbated brain injury during the acute (24\u00a0hr) and subacute phases (6\u00a0days), with a trend toward more severe volume loss in the adult brain. The long\u2010term brain function for coordinated movement and recognition memory, however, were not impacted in the neuronal HIF\u20102\u03b1 deficient mice. Our data suggest that, similar to HIF\u20101\u03b1, neuronal HIF\u20102\u03b1 promotes cell survival in the immature mouse brain. The two HIF alpha isoforms may act through partially overlapping or distinct transcriptional targets to mediate their intrinsic protective responses against neonatal HI brain injury.<\/jats:p>","DOI":"10.1002\/jnr.24943","type":"journal-article","created":{"date-parts":[[2021,9,6]],"date-time":"2021-09-06T16:29:45Z","timestamp":1630945785000},"page":"2964-2975","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Neuronal deficiency of hypoxia\u2010inducible factor 2\u03b1 increases hypoxic\u2010ischemic brain injury in neonatal mice"],"prefix":"10.1002","volume":"99","author":[{"given":"Dawei","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Anesthesiology, the Second Affiliated Hospital, School of Medicine Zhejiang University  Hangzhou China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Fuxin","family":"Lu","sequence":"additional","affiliation":[{"name":"Department of 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