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Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury
Severe cerebral ischemia/reperfusion injury has been shown to induce high-level autophagy and neuronal death. Therefore, it is extremely important to search for a target that inhibits autophagy activation. Long non-coding RNA MEG3 participates in autophagy. However, it remains unclear whether it can...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8530138/ https://www.ncbi.nlm.nih.gov/pubmed/34472482 http://dx.doi.org/10.4103/1673-5374.322466 |
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author | Li, Tian-Hao Sun, Hong-Wei Song, Lai-Jun Yang, Bo Zhang, Peng Yan, Dong-Ming Liu, Xian-Zhi Luo, Yu-Ru |
author_facet | Li, Tian-Hao Sun, Hong-Wei Song, Lai-Jun Yang, Bo Zhang, Peng Yan, Dong-Ming Liu, Xian-Zhi Luo, Yu-Ru |
author_sort | Li, Tian-Hao |
collection | PubMed |
description | Severe cerebral ischemia/reperfusion injury has been shown to induce high-level autophagy and neuronal death. Therefore, it is extremely important to search for a target that inhibits autophagy activation. Long non-coding RNA MEG3 participates in autophagy. However, it remains unclear whether it can be targeted to regulate cerebral ischemia/reperfusion injury. Our results revealed that in oxygen and glucose deprivation/reoxygenation-treated HT22 cells, MEG3 expression was obviously upregulated, and autophagy was increased, while knockdown of MEG3 expression greatly reduced autophagy. Furthermore, MEG3 bound miR-181c-5p and inhibited its expression, while miR-181c-5p bound to autophagy-related gene ATG7 and inhibited its expression. Further experiments revealed that mir-181c-5p overexpression reversed the effect of MEG3 on autophagy and ATG7 expression in HT22 cells subjected to oxygen and glucose deprivation/reoxygenation. In vivo experiments revealed that MEG3 knockdown suppressed autophagy, infarct volume and behavioral deficits in cerebral ischemia/reperfusion mice. These findings suggest that MEG3 knockdown inhibited autophagy and alleviated cerebral ischemia/reperfusion injury through the miR-181c-5p/ATG7 signaling pathway. Therefore, MEG3 can be considered as an intervention target for the treatment of cerebral ischemia/reperfusion injury. This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Zhengzhou University, China (approval No. XF20190538) on January 4, 2019. |
format | Online Article Text |
id | pubmed-8530138 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Wolters Kluwer - Medknow |
record_format | MEDLINE/PubMed |
spelling | pubmed-85301382021-11-09 Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury Li, Tian-Hao Sun, Hong-Wei Song, Lai-Jun Yang, Bo Zhang, Peng Yan, Dong-Ming Liu, Xian-Zhi Luo, Yu-Ru Neural Regen Res Research Article Severe cerebral ischemia/reperfusion injury has been shown to induce high-level autophagy and neuronal death. Therefore, it is extremely important to search for a target that inhibits autophagy activation. Long non-coding RNA MEG3 participates in autophagy. However, it remains unclear whether it can be targeted to regulate cerebral ischemia/reperfusion injury. Our results revealed that in oxygen and glucose deprivation/reoxygenation-treated HT22 cells, MEG3 expression was obviously upregulated, and autophagy was increased, while knockdown of MEG3 expression greatly reduced autophagy. Furthermore, MEG3 bound miR-181c-5p and inhibited its expression, while miR-181c-5p bound to autophagy-related gene ATG7 and inhibited its expression. Further experiments revealed that mir-181c-5p overexpression reversed the effect of MEG3 on autophagy and ATG7 expression in HT22 cells subjected to oxygen and glucose deprivation/reoxygenation. In vivo experiments revealed that MEG3 knockdown suppressed autophagy, infarct volume and behavioral deficits in cerebral ischemia/reperfusion mice. These findings suggest that MEG3 knockdown inhibited autophagy and alleviated cerebral ischemia/reperfusion injury through the miR-181c-5p/ATG7 signaling pathway. Therefore, MEG3 can be considered as an intervention target for the treatment of cerebral ischemia/reperfusion injury. This study was approved by the Animal Ethics Committee of the First Affiliated Hospital of Zhengzhou University, China (approval No. XF20190538) on January 4, 2019. Wolters Kluwer - Medknow 2021-08-30 /pmc/articles/PMC8530138/ /pubmed/34472482 http://dx.doi.org/10.4103/1673-5374.322466 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Research Article Li, Tian-Hao Sun, Hong-Wei Song, Lai-Jun Yang, Bo Zhang, Peng Yan, Dong-Ming Liu, Xian-Zhi Luo, Yu-Ru Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury |
title | Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury |
title_full | Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury |
title_fullStr | Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury |
title_full_unstemmed | Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury |
title_short | Long non-coding RNA MEG3 regulates autophagy after cerebral ischemia/reperfusion injury |
title_sort | long non-coding rna meg3 regulates autophagy after cerebral ischemia/reperfusion injury |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8530138/ https://www.ncbi.nlm.nih.gov/pubmed/34472482 http://dx.doi.org/10.4103/1673-5374.322466 |
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