Involvement of upregulation of miR-210 in a rat epilepsy model

Licheng Chen, Hao Zheng, Shimeng Zhang Neurological Department of Internal Medicine, Linyi People’s Hospital of Shandong Province, Linyi, People’s Republic of China Abstract: Epilepsy is a common type of neurological disorder with complex etiology. The mechanisms are still not...

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Autores principales:	Chen L, Zheng H, Zhang S
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2016
Materias:	Epilepsy miR-210 γ-Aminobutyric acid glutamate decarboxylase γ-Aminobutyric acid transaminase Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/f78634f4371345a09e3d48303ecf3cb3
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spelling	oai:doaj.org-article:f78634f4371345a09e3d48303ecf3cb32021-12-02T04:46:14ZInvolvement of upregulation of miR-210 in a rat epilepsy model1178-2021https://doaj.org/article/f78634f4371345a09e3d48303ecf3cb32016-07-01T00:00:00Zhttps://www.dovepress.com/involvement-of-upregulation-of-mir-210-in-a-rat-epilepsy-model-peer-reviewed-article-NDThttps://doaj.org/toc/1178-2021Licheng Chen, Hao Zheng, Shimeng Zhang Neurological Department of Internal Medicine, Linyi People’s Hospital of Shandong Province, Linyi, People’s Republic of China Abstract: Epilepsy is a common type of neurological disorder with complex etiology. The mechanisms are still not clear. MicroRNAs are endogenous noncoding RNAs with many physiological activities. Multiple microRNAs were abnormally expressed in status epilepticus, including miR-210. In this study, we applied lithium chloride and pilocarpine to induce epileptic activity and aimed to disclose the potential mechanisms. Our data showed that miR-210 was significantly upregulated in hippocampus one day after modeling (P<0.05 vs control) and the high expression of miR-210 lasted for at least 30 days. By contrast, γ-aminobutyric acid (GABA) level significantly decreased concurrently after modeling (P<0.05 vs control). To question whether miR-210 could be a potential therapeutic target for epilepsy, miR-210 inhibitor was administrated through intrahippocampal injection after epilepsy modeling. Our data showed that morphological changes of hippocampal neurons and apoptosis triggered by epilepsy were mitigated by miR-210 inhibition. More importantly, the expressions of GABA-related proteins, including GABAA receptor α1, glutamate decarboxylase, and GABA transporter 1, were significantly elevated after epilepsy modeling in both mRNA and protein levels 3 days postmodeling (P<0.05 vs control), which were mitigated by miR-210 inhibitor treatment (P<0.05 vs model). In addition, epilepsy-induced upregulation of GABA transaminase was alleviated by miR-210 inhibitor. Taken together, these data implicated potential roles of miR-210 in lithium chloride–pilocarpine-induced epilepsy model and miR-210 could serve as a potential therapeutic target in status epilepticus. Keywords: epilepsy, miR-210, γ-aminobutyric acid, glutamate decarboxylase, γ-aminobutyric acid transaminaseChen LZheng HZhang SDove Medical PressarticleEpilepsymiR-210γ-Aminobutyric acidglutamate decarboxylaseγ-Aminobutyric acid transaminaseNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol 2016, Iss Issue 1, Pp 1731-1737 (2016)
institution	DOAJ
collection	DOAJ
language	EN
topic	Epilepsy miR-210 γ-Aminobutyric acid glutamate decarboxylase γ-Aminobutyric acid transaminase Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
spellingShingle	Epilepsy miR-210 γ-Aminobutyric acid glutamate decarboxylase γ-Aminobutyric acid transaminase Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Chen L Zheng H Zhang S Involvement of upregulation of miR-210 in a rat epilepsy model
description	Licheng Chen, Hao Zheng, Shimeng Zhang Neurological Department of Internal Medicine, Linyi People’s Hospital of Shandong Province, Linyi, People’s Republic of China Abstract: Epilepsy is a common type of neurological disorder with complex etiology. The mechanisms are still not clear. MicroRNAs are endogenous noncoding RNAs with many physiological activities. Multiple microRNAs were abnormally expressed in status epilepticus, including miR-210. In this study, we applied lithium chloride and pilocarpine to induce epileptic activity and aimed to disclose the potential mechanisms. Our data showed that miR-210 was significantly upregulated in hippocampus one day after modeling (P<0.05 vs control) and the high expression of miR-210 lasted for at least 30 days. By contrast, γ-aminobutyric acid (GABA) level significantly decreased concurrently after modeling (P<0.05 vs control). To question whether miR-210 could be a potential therapeutic target for epilepsy, miR-210 inhibitor was administrated through intrahippocampal injection after epilepsy modeling. Our data showed that morphological changes of hippocampal neurons and apoptosis triggered by epilepsy were mitigated by miR-210 inhibition. More importantly, the expressions of GABA-related proteins, including GABAA receptor α1, glutamate decarboxylase, and GABA transporter 1, were significantly elevated after epilepsy modeling in both mRNA and protein levels 3 days postmodeling (P<0.05 vs control), which were mitigated by miR-210 inhibitor treatment (P<0.05 vs model). In addition, epilepsy-induced upregulation of GABA transaminase was alleviated by miR-210 inhibitor. Taken together, these data implicated potential roles of miR-210 in lithium chloride–pilocarpine-induced epilepsy model and miR-210 could serve as a potential therapeutic target in status epilepticus. Keywords: epilepsy, miR-210, γ-aminobutyric acid, glutamate decarboxylase, γ-aminobutyric acid transaminase
format	article
author	Chen L Zheng H Zhang S
author_facet	Chen L Zheng H Zhang S
author_sort	Chen L
title	Involvement of upregulation of miR-210 in a rat epilepsy model
title_short	Involvement of upregulation of miR-210 in a rat epilepsy model
title_full	Involvement of upregulation of miR-210 in a rat epilepsy model
title_fullStr	Involvement of upregulation of miR-210 in a rat epilepsy model
title_full_unstemmed	Involvement of upregulation of miR-210 in a rat epilepsy model
title_sort	involvement of upregulation of mir-210 in a rat epilepsy model
publisher	Dove Medical Press
publishDate	2016
url	https://doaj.org/article/f78634f4371345a09e3d48303ecf3cb3
work_keys_str_mv	AT chenl involvementofupregulationofmir210inaratepilepsymodel AT zhengh involvementofupregulationofmir210inaratepilepsymodel AT zhangs involvementofupregulationofmir210inaratepilepsymodel
_version_	1718401075268026368

Involvement of upregulation of miR-210 in a rat epilepsy model

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