Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG

LncRNAs are identified as critical regulators in cerebral ischemia/reperfusion injury (CIRI). In this current work, SH-SY5Y cells suffered from oxygen-glucose deprivation/reperfusion (OGD/R) were applied to analyze the biological role of lncRNA NORAD and underlying molecular mechanism in CIRI in vit...

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Autores principales:	Xinyu Zhou, Zhonglong Wang, Bingchao Xu, Niu Ji, Pin Meng, Lei Gu, Ying Li
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	lncrna norad mir-30a-5p ywhag ogd/r injury cerebral ischemia/reperfusion injury Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/3ada8bdce65c411b9339c812906adc51
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spelling	oai:doaj.org-article:3ada8bdce65c411b9339c812906adc512021-11-26T11:19:49ZLong non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG2165-59792165-598710.1080/21655979.2021.1995115https://doaj.org/article/3ada8bdce65c411b9339c812906adc512021-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1995115https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987LncRNAs are identified as critical regulators in cerebral ischemia/reperfusion injury (CIRI). In this current work, SH-SY5Y cells suffered from oxygen-glucose deprivation/reperfusion (OGD/R) were applied to analyze the biological role of lncRNA NORAD and underlying molecular mechanism in CIRI in vitro. Levels of lncRNA NORAD, miR-30a-5p and YWHAG were measured using RT-qPCR. Bioinformatics analysis predicted the binding sites of lncRNA NORAD to miR-30a-5p and miR-30a-5p to YWHAG. Luciferase reporter assay verified the binding relationships among lncRNA NORAD, miR-30a-5p and YWHAG. Additionally, cell viability was determined using CCK-8 assay, and cell apoptosis was assessed using TUNEL staining and western blot analysis. Moreover, the levels of ROS, MDA, LDH and SOD as well as IL-1β, TNF-α, and IL-6 were assessed via application of the corresponding assay kits. Decreased cell viability and temporarily increased lncRNA NORAD level were observed in SH-SY5Y cells after OGD/R. It was demonstrated that lncRNA NORAD regulated YWHAG expression by sponging miR-30a-5p. Upregulation of lncRNA NORAD contributed to the enhancement of cell viability, the inhibition of cell apoptosis as well as the alleviation of oxidative stress and inflammation in OGD/R-injured SH-SY5Y cells, which were reversed upon elevation of miR-30a-5p. In contrast, downregulation of lncRNA NORAD reduced cell viability, promoted cell apoptosis as well as aggravated oxidative stress and inflammation under OGD/R challenge, and the functions of lncRNA NORAD knockdown in OGD/R injury were abolished by upregulation of YWHAG. Taken together, lncRNA NORAD exerted protective effects against OGD/R-induced neural injury by sponging miR-30a-5p to upregulate YWHAG expression.Xinyu ZhouZhonglong WangBingchao XuNiu JiPin MengLei GuYing LiTaylor & Francis Grouparticlelncrna noradmir-30a-5pywhagogd/r injurycerebral ischemia/reperfusion injuryBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 2, Pp 9174-9188 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	lncrna norad mir-30a-5p ywhag ogd/r injury cerebral ischemia/reperfusion injury Biotechnology TP248.13-248.65
spellingShingle	lncrna norad mir-30a-5p ywhag ogd/r injury cerebral ischemia/reperfusion injury Biotechnology TP248.13-248.65 Xinyu Zhou Zhonglong Wang Bingchao Xu Niu Ji Pin Meng Lei Gu Ying Li Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG
description	LncRNAs are identified as critical regulators in cerebral ischemia/reperfusion injury (CIRI). In this current work, SH-SY5Y cells suffered from oxygen-glucose deprivation/reperfusion (OGD/R) were applied to analyze the biological role of lncRNA NORAD and underlying molecular mechanism in CIRI in vitro. Levels of lncRNA NORAD, miR-30a-5p and YWHAG were measured using RT-qPCR. Bioinformatics analysis predicted the binding sites of lncRNA NORAD to miR-30a-5p and miR-30a-5p to YWHAG. Luciferase reporter assay verified the binding relationships among lncRNA NORAD, miR-30a-5p and YWHAG. Additionally, cell viability was determined using CCK-8 assay, and cell apoptosis was assessed using TUNEL staining and western blot analysis. Moreover, the levels of ROS, MDA, LDH and SOD as well as IL-1β, TNF-α, and IL-6 were assessed via application of the corresponding assay kits. Decreased cell viability and temporarily increased lncRNA NORAD level were observed in SH-SY5Y cells after OGD/R. It was demonstrated that lncRNA NORAD regulated YWHAG expression by sponging miR-30a-5p. Upregulation of lncRNA NORAD contributed to the enhancement of cell viability, the inhibition of cell apoptosis as well as the alleviation of oxidative stress and inflammation in OGD/R-injured SH-SY5Y cells, which were reversed upon elevation of miR-30a-5p. In contrast, downregulation of lncRNA NORAD reduced cell viability, promoted cell apoptosis as well as aggravated oxidative stress and inflammation under OGD/R challenge, and the functions of lncRNA NORAD knockdown in OGD/R injury were abolished by upregulation of YWHAG. Taken together, lncRNA NORAD exerted protective effects against OGD/R-induced neural injury by sponging miR-30a-5p to upregulate YWHAG expression.
format	article
author	Xinyu Zhou Zhonglong Wang Bingchao Xu Niu Ji Pin Meng Lei Gu Ying Li
author_facet	Xinyu Zhou Zhonglong Wang Bingchao Xu Niu Ji Pin Meng Lei Gu Ying Li
author_sort	Xinyu Zhou
title	Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG
title_short	Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG
title_full	Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG
title_fullStr	Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG
title_full_unstemmed	Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG
title_sort	long non-coding rna norad protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating mir-30a-5p/ywhag
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/3ada8bdce65c411b9339c812906adc51
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Long non-coding RNA NORAD protects against cerebral ischemia/reperfusion injury induced brain damage, cell apoptosis, oxidative stress and inflammation by regulating miR-30a-5p/YWHAG

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