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miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury
The present study aimed to determine whether an miRNA (miR)-29b inhibitor protected against cerebral ischemia/reperfusion (I/R) injury in vitro and to investigate the underlying mechanisms. As a model for induced cerebral IR injury, N2a cells were exposed to an oxygen-glucose deprivation/reoxygenati...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143871/ https://www.ncbi.nlm.nih.gov/pubmed/30233687 http://dx.doi.org/10.3892/etm.2018.6622 |
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author | Huang, Zhi Lu, Lu Jiang, Tianpeng Zhang, Shuai Shen, Yaping Zheng, Zhu Zhao, Ansu Gao, Rui Li, Rui Zhou, Shi Liu, Jing |
author_facet | Huang, Zhi Lu, Lu Jiang, Tianpeng Zhang, Shuai Shen, Yaping Zheng, Zhu Zhao, Ansu Gao, Rui Li, Rui Zhou, Shi Liu, Jing |
author_sort | Huang, Zhi |
collection | PubMed |
description | The present study aimed to determine whether an miRNA (miR)-29b inhibitor protected against cerebral ischemia/reperfusion (I/R) injury in vitro and to investigate the underlying mechanisms. As a model for induced cerebral IR injury, N2a cells were exposed to an oxygen-glucose deprivation/reoxygenation (OGD/R) environment. Using this model, it was demonstrated that miR-29b was significantly upregulated compared with cells in a normal environment. The interactions between miR-29b and myeloid cell leukemia sequence (MCL)-1 were then investigated using dual-luciferase assays, revealing a strong regulation of MCL-1 through the 3′untranslated region. Using the OGD/R model, the present study additionally examined the effects of miR-29b and miR-29b inhibitor on cell viability and apoptosis using Cell Counting kit 8 and flow cytometry assays, respectively. miR-29b transfection led to increased N2a cell apoptosis and reduced cell viability under an OGD/R environment. However, this effect was reversed by the miR-29b inhibitor. Finally, the effects of miR-29b on the expression of several Wnt-associating proteins were examined. It was observed that B cell lymphoma-2 was inhibited by miR-29b, as was MCL-1, whereas caspase-3 expression was promoted. The miR-29b inhibitor demonstrated the opposite effect. Overall, miR-29b promoted neurocyte apoptosis by targeting MCL-1 during cerebral I/R injury. The results of the present study suggest a potential novel therapeutic target for the treatment of ischemic stroke. |
format | Online Article Text |
id | pubmed-6143871 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-61438712018-09-19 miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury Huang, Zhi Lu, Lu Jiang, Tianpeng Zhang, Shuai Shen, Yaping Zheng, Zhu Zhao, Ansu Gao, Rui Li, Rui Zhou, Shi Liu, Jing Exp Ther Med Articles The present study aimed to determine whether an miRNA (miR)-29b inhibitor protected against cerebral ischemia/reperfusion (I/R) injury in vitro and to investigate the underlying mechanisms. As a model for induced cerebral IR injury, N2a cells were exposed to an oxygen-glucose deprivation/reoxygenation (OGD/R) environment. Using this model, it was demonstrated that miR-29b was significantly upregulated compared with cells in a normal environment. The interactions between miR-29b and myeloid cell leukemia sequence (MCL)-1 were then investigated using dual-luciferase assays, revealing a strong regulation of MCL-1 through the 3′untranslated region. Using the OGD/R model, the present study additionally examined the effects of miR-29b and miR-29b inhibitor on cell viability and apoptosis using Cell Counting kit 8 and flow cytometry assays, respectively. miR-29b transfection led to increased N2a cell apoptosis and reduced cell viability under an OGD/R environment. However, this effect was reversed by the miR-29b inhibitor. Finally, the effects of miR-29b on the expression of several Wnt-associating proteins were examined. It was observed that B cell lymphoma-2 was inhibited by miR-29b, as was MCL-1, whereas caspase-3 expression was promoted. The miR-29b inhibitor demonstrated the opposite effect. Overall, miR-29b promoted neurocyte apoptosis by targeting MCL-1 during cerebral I/R injury. The results of the present study suggest a potential novel therapeutic target for the treatment of ischemic stroke. D.A. Spandidos 2018-10 2018-08-20 /pmc/articles/PMC6143871/ /pubmed/30233687 http://dx.doi.org/10.3892/etm.2018.6622 Text en Copyright: © Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Huang, Zhi Lu, Lu Jiang, Tianpeng Zhang, Shuai Shen, Yaping Zheng, Zhu Zhao, Ansu Gao, Rui Li, Rui Zhou, Shi Liu, Jing miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury |
title | miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury |
title_full | miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury |
title_fullStr | miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury |
title_full_unstemmed | miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury |
title_short | miR-29b affects neurocyte apoptosis by targeting MCL-1 during cerebral ischemia/reperfusion injury |
title_sort | mir-29b affects neurocyte apoptosis by targeting mcl-1 during cerebral ischemia/reperfusion injury |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143871/ https://www.ncbi.nlm.nih.gov/pubmed/30233687 http://dx.doi.org/10.3892/etm.2018.6622 |
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