{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T14:37:28Z","timestamp":1783953448466,"version":"3.55.0"},"reference-count":36,"publisher":"Wiley","issue":"21","license":[{"start":{"date-parts":[[2021,10,22]],"date-time":"2021-10-22T00:00:00Z","timestamp":1634860800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2021,11]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Long non\u2010coding RNA (lncRNA) <jats:italic>MIAT<\/jats:italic> (myocardial infarction associated transcript) has been characterized as a functional lncRNA modulating cerebral ischaemic\/reperfusion (I\/R) injury. However, the underlying mechanisms remain poorly understood. This study explored the functional partners of <jats:italic>MIAT<\/jats:italic> in primary rat neurons and their regulation on I\/R injury. Sprague\u2010Dawley rats were used to construct middle cerebral artery occlusion (MCAO) models. Their cerebral cortical neurons were used for <jats:italic>in vitro<\/jats:italic> oxygen\u2010glucose deprivation\/reoxygenation (OGD\/R) models. Results showed that <jats:italic>MIAT<\/jats:italic> interacted with EGLN2 in rat cortical neurons. <jats:italic>MIAT<\/jats:italic> overexpression or knockdown did not alter <jats:italic>EGLN2<\/jats:italic> transcription. In contrast, <jats:italic>MIAT<\/jats:italic> overexpression increased EGLN2\u00a0stability after I\/R injury via reducing its ubiquitin\u2010mediated degradation. EGLN2 was a substrate of MDM2, a ubiquitin E3\u00a0ligase. MDM2 interacted with the N\u2010terminal of EGLN2 and mediated its K48\u2010linked poly\u2010ubiquitination, thereby facilitating its proteasomal degradation. <jats:italic>MIAT<\/jats:italic> knockdown enhanced the interaction and reduced EGLN2\u00a0stability. <jats:italic>MIAT<\/jats:italic> overexpression enhanced infarct volume and induced a higher ratio of neuronal apoptosis. <jats:italic>EGLN2<\/jats:italic>\u00a0knockdown significantly reversed the injury. <jats:italic>MIAT<\/jats:italic> overexpression reduced oxidative pentose phosphate pathway flux and increased oxidized\/reduced glutathione ratio, the effects of which were abrogated by <jats:italic>EGLN2<\/jats:italic>\u00a0knockdown. In conclusion, <jats:italic>MIAT<\/jats:italic> might act as a stabilizer of EGLN2 via reducing MDM2\u00a0mediated K48 poly\u2010ubiquitination. <jats:italic>MIAT<\/jats:italic>\u2010EGLN2 axis exacerbates I\/R injury via altering redox homeostasis in neurons.<\/jats:p>","DOI":"10.1111\/jcmm.16950","type":"journal-article","created":{"date-parts":[[2021,10,23]],"date-time":"2021-10-23T06:19:55Z","timestamp":1634969995000},"page":"10140-10151","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["LncRNA <i>MIAT<\/i> enhances cerebral ischaemia\/reperfusion injury in rat model via interacting with EGLN2 and reduces its ubiquitin\u2010mediated degradation"],"prefix":"10.1111","volume":"25","author":[{"given":"Suping","family":"Li","sequence":"first","affiliation":[{"name":"Department of Neurology Sichuan Academy of Medical Sciences &amp; Sichuan Provincial People's Hospital Chengdu 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