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miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4

Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR-29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4...

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Autores principales: Zheng, Yueying, Pan, Caifei, Chen, Manli, Pei, Aijie, Xie, Liwei, Zhu, Shengmei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365700/
https://www.ncbi.nlm.nih.gov/pubmed/30628716
http://dx.doi.org/10.3892/or.2019.6961
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author Zheng, Yueying
Pan, Caifei
Chen, Manli
Pei, Aijie
Xie, Liwei
Zhu, Shengmei
author_facet Zheng, Yueying
Pan, Caifei
Chen, Manli
Pei, Aijie
Xie, Liwei
Zhu, Shengmei
author_sort Zheng, Yueying
collection PubMed
description Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR-29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4 (AQP4). Real-time PCR and western blotting were used to assess miR-29a levels and AQP4 protein levels, respectively. Apoptosis was detected by flow cytometry, and lactate dehydrogenase (LDH) was determined by enzyme-linked immunosorbent assay (ELISA). Overexpression of miR-29a was significantly downregulated in OGD-induced primary astrocytes, and transfection with a miR-29a mimic decreased LDH release and apoptosis, and improved cell health in OGD-induced astrocytes. AQP4 was the target of miR-29a, which suppressed AQP4 expression, and knockdown of AQP4 mitigated OGD-induced astrocyte injury. Furthermore, miR-29a regulated AQP4 expression in OGD-induced astrocytes. AQP4 exacerbated astrocyte injury following ischemic stroke, and knockdown of AQP4 protected OGD/RX-induced primary cultured astrocytes against injury. The effect of miR-29a inhibitor on primary astrocytes was lost following AQP4 knockdown. These findings indicated that miR-29a prevented astrocyte injury in vitro by inhibiting AQP4. Thus, miR-29a may protect primary cultured astrocytes after OGD-induced injury by targeting AQP4, and may be a potential therapeutic target for ischemic injury of astrocytes.
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spelling pubmed-63657002019-02-23 miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4 Zheng, Yueying Pan, Caifei Chen, Manli Pei, Aijie Xie, Liwei Zhu, Shengmei Oncol Rep Articles Ischemic stroke is the main cause of brain injury and results in a high rate of morbidity, disability and mortality. In the present study, we aimed to determine whether miR-29a played a protective role in oxygen glucose deprivation (OGD) injury via regulation of the water channel protein aquaporin 4 (AQP4). Real-time PCR and western blotting were used to assess miR-29a levels and AQP4 protein levels, respectively. Apoptosis was detected by flow cytometry, and lactate dehydrogenase (LDH) was determined by enzyme-linked immunosorbent assay (ELISA). Overexpression of miR-29a was significantly downregulated in OGD-induced primary astrocytes, and transfection with a miR-29a mimic decreased LDH release and apoptosis, and improved cell health in OGD-induced astrocytes. AQP4 was the target of miR-29a, which suppressed AQP4 expression, and knockdown of AQP4 mitigated OGD-induced astrocyte injury. Furthermore, miR-29a regulated AQP4 expression in OGD-induced astrocytes. AQP4 exacerbated astrocyte injury following ischemic stroke, and knockdown of AQP4 protected OGD/RX-induced primary cultured astrocytes against injury. The effect of miR-29a inhibitor on primary astrocytes was lost following AQP4 knockdown. These findings indicated that miR-29a prevented astrocyte injury in vitro by inhibiting AQP4. Thus, miR-29a may protect primary cultured astrocytes after OGD-induced injury by targeting AQP4, and may be a potential therapeutic target for ischemic injury of astrocytes. D.A. Spandidos 2019-03 2019-01-09 /pmc/articles/PMC6365700/ /pubmed/30628716 http://dx.doi.org/10.3892/or.2019.6961 Text en Copyright: © Zheng 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
Zheng, Yueying
Pan, Caifei
Chen, Manli
Pei, Aijie
Xie, Liwei
Zhu, Shengmei
miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
title miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
title_full miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
title_fullStr miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
title_full_unstemmed miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
title_short miR-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
title_sort mir-29a ameliorates ischemic injury of astrocytes in vitro by targeting the water channel protein aquaporin 4
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6365700/
https://www.ncbi.nlm.nih.gov/pubmed/30628716
http://dx.doi.org/10.3892/or.2019.6961
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