{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T23:27:54Z","timestamp":1782948474794,"version":"3.54.5"},"reference-count":34,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2022,7,21]],"date-time":"2022-07-21T00:00:00Z","timestamp":1658361600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ibrain"],"published-print":{"date-parts":[[2022,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Neonatal hypoxic\u2010ischemic encephalopathy (NHIE) is one of the major diseases in newborns during the perinatal stage, which\u00a0globally is the main reason for children's\u00a0morbidity and mortality. However, the mechanism of NHIE still remains poorly clear. In this study, the 7\u2010day\u2010old rats were subjected to hypoxic\u2010ischemia (HI), then brain damage was detected. Afterward, the expression of eva\u20101 homolog C (EVA1C) was measured in vitro by establishing the\u00a0oxygen\u2010glucose deprivation (OGD) model in SHSY5Y cells and human fetal neurons. Subsequently, the potential function and mechanism of EVA1C were explored by silencing EVA1C and alternative splicing prediction. As a result, obvious neurobehavioral impairment and brain infarction were detected through Zea\u2010Longa score and TTC staining; meanwhile, neuron injury was tested by HE and Nissl staining post HI. Moreover, it was found that the expression of EVA1C was notably upregulated in SHSY5Y cells and human fetal neurons after OGD. In addition, cell survival and growth were increased after silencing EVA1C, which might be associated with alternative splicing. In conclusion, EVA1C interference exhibited potential in promoting neuron survival and growth, associated with exon skipping with the alternative splicing site in 34613318:34687258, which may provide the basis for the therapeutic target and mechanism research of NHIE.<\/jats:p>","DOI":"10.1002\/ibra.12053","type":"journal-article","created":{"date-parts":[[2022,7,21]],"date-time":"2022-07-21T09:49:47Z","timestamp":1658396987000},"page":"481-491","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Downregulating EVA1C exerts the potential to promote neuron growth after neonatal hypoxic\u2010ischemic encephalopathy injury associated with alternative splicing"],"prefix":"10.1002","volume":"8","author":[{"given":"Yue","family":"Hu","sequence":"first","affiliation":[{"name":"Department of Anesthesia Operation The First People's Hospital of Shuangliu District  Chengdu Sichuan 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