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The cerebral infarct volume and neurological impairment were assessed using 2,3,5\u2010triphenyl\u2010tetrazolium chloride staining and neurobehavioral tests, respectively. Relevant proteins were evaluated using western blotting and immunofluorescence staining. Additionally, a bioinformatics website was used to predict the potential target genes of lncRNA H19. Finally, a rescue experiment was conducted to confirm the potential mechanism.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Silencing of H19 significantly decreased the cerebral infarct volume, enhanced the recovery of neurological function, mitigated BBB damage, and stimulated endothelial cell proliferation following ischemic stroke. Insulin\u2010like growth factor 2 mRNA\u2010binding protein 2 (IMP2) is predicted to be a potential target gene for lncRNA H19. H19 knockdown increased IMP2 protein expression and IMP2 inhibition reversed the protective effects of H19 inhibition.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Downregulation of H19 enhances angiogenesis and mitigates BBB damage by regulating IMP2, thereby alleviating cerebral I\/R injury.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.70000","type":"journal-article","created":{"date-parts":[[2024,8,20]],"date-time":"2024-08-20T06:06:38Z","timestamp":1724133998000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Long noncoding <scp>RNA H19<\/scp> knockdown promotes angiogenesis via <scp>IMP2<\/scp> after ischemic stroke"],"prefix":"10.1111","volume":"30","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-5511-6432","authenticated-orcid":false,"given":"Liyuan","family":"Zhong","sequence":"first","affiliation":[{"name":"Institute of Cerebrovascular Disease Research and Department of 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