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By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice

Neuronal apoptosis was considered as one of the main factors of cerebral ischemia/reperfusion injury. Understanding the molecular regulatory mechanism of neuronal apoptosis under the cerebral ischemia/reperfusion injury may provide the novel therapeutic targets for cerebral ischemia/reperfusion inju...

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Autores principales: Liu, Xindong, Wang, Xin, Zhang, Lijuan, Zhou, Yi, Yang, Le, Yang, Minghao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806345/
https://www.ncbi.nlm.nih.gov/pubmed/33724167
http://dx.doi.org/10.1080/21655979.2021.1898134
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author Liu, Xindong
Wang, Xin
Zhang, Lijuan
Zhou, Yi
Yang, Le
Yang, Minghao
author_facet Liu, Xindong
Wang, Xin
Zhang, Lijuan
Zhou, Yi
Yang, Le
Yang, Minghao
author_sort Liu, Xindong
collection PubMed
description Neuronal apoptosis was considered as one of the main factors of cerebral ischemia/reperfusion injury. Understanding the molecular regulatory mechanism of neuronal apoptosis under the cerebral ischemia/reperfusion injury may provide the novel therapeutic targets for cerebral ischemia/reperfusion injury. However, the molecular regulatory mechanism of neurons fate determination under the cerebral ischemia/reperfusion injury remains poorly understood. This study was aimed to delve into the related molecular mechanism of miR-484 on the regulation of cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice. In this study, quantitative real-time polymerase chain reaction assays revealed that the expression level of miR-484 was down-regulated in neurons following OGD. Then, CCK8 assay western blot assay, and flow cytometry assay verified that upregulation of miR-484 increased viability and inhibited apoptosis of neurons following OGD. Further bioinformatics methods and dual-luciferase reporter assay were applied together to anticipate and certify the interaction between miR-484 and BCL2L13. Finally, cerebral infarct size assessment and TUNEL staining confirmed that overexpression of miR-484 alleviated cerebral ischemia/reperfusion injury in mice, and overexpression of BCL2L13 could abolish the effect of miR-484-suppressed cell apoptosis. All these results suggested that miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice by targeting apoptosis facilitator BCL2L13.
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spelling pubmed-88063452022-02-02 By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice Liu, Xindong Wang, Xin Zhang, Lijuan Zhou, Yi Yang, Le Yang, Minghao Bioengineered Research Paper Neuronal apoptosis was considered as one of the main factors of cerebral ischemia/reperfusion injury. Understanding the molecular regulatory mechanism of neuronal apoptosis under the cerebral ischemia/reperfusion injury may provide the novel therapeutic targets for cerebral ischemia/reperfusion injury. However, the molecular regulatory mechanism of neurons fate determination under the cerebral ischemia/reperfusion injury remains poorly understood. This study was aimed to delve into the related molecular mechanism of miR-484 on the regulation of cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice. In this study, quantitative real-time polymerase chain reaction assays revealed that the expression level of miR-484 was down-regulated in neurons following OGD. Then, CCK8 assay western blot assay, and flow cytometry assay verified that upregulation of miR-484 increased viability and inhibited apoptosis of neurons following OGD. Further bioinformatics methods and dual-luciferase reporter assay were applied together to anticipate and certify the interaction between miR-484 and BCL2L13. Finally, cerebral infarct size assessment and TUNEL staining confirmed that overexpression of miR-484 alleviated cerebral ischemia/reperfusion injury in mice, and overexpression of BCL2L13 could abolish the effect of miR-484-suppressed cell apoptosis. All these results suggested that miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice by targeting apoptosis facilitator BCL2L13. Taylor & Francis 2021-03-16 /pmc/articles/PMC8806345/ /pubmed/33724167 http://dx.doi.org/10.1080/21655979.2021.1898134 Text en © 2021 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Liu, Xindong
Wang, Xin
Zhang, Lijuan
Zhou, Yi
Yang, Le
Yang, Minghao
By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
title By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
title_full By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
title_fullStr By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
title_full_unstemmed By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
title_short By targeting apoptosis facilitator BCL2L13, microRNA miR-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
title_sort by targeting apoptosis facilitator bcl2l13, microrna mir-484 alleviates cerebral ischemia/reperfusion injury-induced neuronal apoptosis in mice
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8806345/
https://www.ncbi.nlm.nih.gov/pubmed/33724167
http://dx.doi.org/10.1080/21655979.2021.1898134
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