HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis

Abstract Stroke is a common cause of death worldwide and leads to disability and cognitive dysfunction. Ischemic stroke and hemorrhagic stroke are major categories of stroke, accounting for 68% and 32% of strokes, respectively. Each year, 15 million people experience stroke worldwide, and the stroke...

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Autores principales:	Jui-Sheng Chen, Hao-Kuang Wang, Chien-Yu Hsu, Yu-Ting Su, Jia-Shing Chen, Cheng-Loong Liang, Patrick Ching-Ho Hsieh, Cheng-Chun Wu, Aij-Lie Kwan
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/06f868f8eed54cb4ad8a1c0892db04b0
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spelling	oai:doaj.org-article:06f868f8eed54cb4ad8a1c0892db04b02021-12-02T15:08:11ZHDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis10.1038/s41598-021-95837-32045-2322https://doaj.org/article/06f868f8eed54cb4ad8a1c0892db04b02021-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-95837-3https://doaj.org/toc/2045-2322Abstract Stroke is a common cause of death worldwide and leads to disability and cognitive dysfunction. Ischemic stroke and hemorrhagic stroke are major categories of stroke, accounting for 68% and 32% of strokes, respectively. Each year, 15 million people experience stroke worldwide, and the stroke incidence is rising. Epigenetic modifications regulate gene transcription and play a major role in stroke. Accordingly, histone deacetylase 1 (HDAC1) participates in DNA damage repair and cell survival. However, the mechanisms underlying the role of HDAC1 in stroke pathogenesis are still controversial. Therefore, we investigated the role of HDAC1 in stroke by using a rat model of endothelin-1-induced brain ischemia. Our results revealed that HDAC1 was deregulated following stroke, and its expressional level and enzymatic activity were decreased. We also used MS-275 to inhibit HDAC1 function in rats exposed to ischemic insult. We found that HDAC1 inhibition promoted the infarct volume, neuronal loss, DNA damage, neuronal apoptosis after stroke, and levels of reactive oxygen species and inflammation cytokines. Additionally, HDAC1 inhibition deteriorated the behavioral outcomes of rats with ischemic insult. Overall, our findings demonstrate that HDAC1 participates in ischemic pathogenesis in the brain and possesses potential for use as a therapeutic target.Jui-Sheng ChenHao-Kuang WangChien-Yu HsuYu-Ting SuJia-Shing ChenCheng-Loong LiangPatrick Ching-Ho HsiehCheng-Chun WuAij-Lie KwanNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-11 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jui-Sheng Chen Hao-Kuang Wang Chien-Yu Hsu Yu-Ting Su Jia-Shing Chen Cheng-Loong Liang Patrick Ching-Ho Hsieh Cheng-Chun Wu Aij-Lie Kwan HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
description	Abstract Stroke is a common cause of death worldwide and leads to disability and cognitive dysfunction. Ischemic stroke and hemorrhagic stroke are major categories of stroke, accounting for 68% and 32% of strokes, respectively. Each year, 15 million people experience stroke worldwide, and the stroke incidence is rising. Epigenetic modifications regulate gene transcription and play a major role in stroke. Accordingly, histone deacetylase 1 (HDAC1) participates in DNA damage repair and cell survival. However, the mechanisms underlying the role of HDAC1 in stroke pathogenesis are still controversial. Therefore, we investigated the role of HDAC1 in stroke by using a rat model of endothelin-1-induced brain ischemia. Our results revealed that HDAC1 was deregulated following stroke, and its expressional level and enzymatic activity were decreased. We also used MS-275 to inhibit HDAC1 function in rats exposed to ischemic insult. We found that HDAC1 inhibition promoted the infarct volume, neuronal loss, DNA damage, neuronal apoptosis after stroke, and levels of reactive oxygen species and inflammation cytokines. Additionally, HDAC1 inhibition deteriorated the behavioral outcomes of rats with ischemic insult. Overall, our findings demonstrate that HDAC1 participates in ischemic pathogenesis in the brain and possesses potential for use as a therapeutic target.
format	article
author	Jui-Sheng Chen Hao-Kuang Wang Chien-Yu Hsu Yu-Ting Su Jia-Shing Chen Cheng-Loong Liang Patrick Ching-Ho Hsieh Cheng-Chun Wu Aij-Lie Kwan
author_facet	Jui-Sheng Chen Hao-Kuang Wang Chien-Yu Hsu Yu-Ting Su Jia-Shing Chen Cheng-Loong Liang Patrick Ching-Ho Hsieh Cheng-Chun Wu Aij-Lie Kwan
author_sort	Jui-Sheng Chen
title	HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
title_short	HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
title_full	HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
title_fullStr	HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
title_full_unstemmed	HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
title_sort	hdac1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/06f868f8eed54cb4ad8a1c0892db04b0
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HDAC1 deregulation promotes neuronal loss and deficit of motor function in stroke pathogenesis

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