Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells

Abstract Amyloid β-protein (Aβ) is believed to contribute to the development of Alzheimer’s disease (AD). Here we showed that Aβ25-35 rapidly caused activation of autophagy, subsequently leading to reduction of autophagy associated with cellular apoptosis. Further investigation revealed that the acc...

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Autores principales:	Yi-qing Liu, Meng-qi Jia, Zhao-hong Xie, Xiao-fei Liu, Hui-Yang, Xiao-lei Zheng, Hui-qing Yuan, Jian-zhong Bi
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/67019f06892b4c4e970964bf203f83e3
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spelling	oai:doaj.org-article:67019f06892b4c4e970964bf203f83e32021-12-02T11:53:07ZArrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells10.1038/s41598-017-01798-x2045-2322https://doaj.org/article/67019f06892b4c4e970964bf203f83e32017-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-01798-xhttps://doaj.org/toc/2045-2322Abstract Amyloid β-protein (Aβ) is believed to contribute to the development of Alzheimer’s disease (AD). Here we showed that Aβ25-35 rapidly caused activation of autophagy, subsequently leading to reduction of autophagy associated with cellular apoptosis. Further investigation revealed that the accumulation of β-arrestin 1 (ARRB1) caused by Aβ25-35 contributed to the induction of autophagic flux. The depletion of ARRB1 led to decreases in the expression of LC3B, Atg7, and Beclin-1, which are essential for the initiation of autophagy. ARRB1 depletion also reduced downstream ERK activity and promoted Aβ25-35-induced cell death. As with ARRB1, transient upregulation of ARRB2 by Aβ25-35 was observed after short treatment durations, whereas genetic reduction of ARRB2 caused a marked increase in the expression of the α7nAch receptor at the cell surface, which resulted in partial reversal of Aβ25-35-induced cell death. Although expression of both ARRB1 and ARRB2 was reduced in serum from patients with AD, the levels of ARRB1 were much lower than those of ARRB2 in AD. Thus, our findings indicate that ARRB1/2 play different roles in Aβ25-35 cytotoxicity, which may provide additional support for exploring the underlying molecular mechanism of AD.Yi-qing LiuMeng-qi JiaZhao-hong XieXiao-fei LiuHui-YangXiao-lei ZhengHui-qing YuanJian-zhong BiNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Yi-qing Liu Meng-qi Jia Zhao-hong Xie Xiao-fei Liu Hui-Yang Xiao-lei Zheng Hui-qing Yuan Jian-zhong Bi Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells
description	Abstract Amyloid β-protein (Aβ) is believed to contribute to the development of Alzheimer’s disease (AD). Here we showed that Aβ25-35 rapidly caused activation of autophagy, subsequently leading to reduction of autophagy associated with cellular apoptosis. Further investigation revealed that the accumulation of β-arrestin 1 (ARRB1) caused by Aβ25-35 contributed to the induction of autophagic flux. The depletion of ARRB1 led to decreases in the expression of LC3B, Atg7, and Beclin-1, which are essential for the initiation of autophagy. ARRB1 depletion also reduced downstream ERK activity and promoted Aβ25-35-induced cell death. As with ARRB1, transient upregulation of ARRB2 by Aβ25-35 was observed after short treatment durations, whereas genetic reduction of ARRB2 caused a marked increase in the expression of the α7nAch receptor at the cell surface, which resulted in partial reversal of Aβ25-35-induced cell death. Although expression of both ARRB1 and ARRB2 was reduced in serum from patients with AD, the levels of ARRB1 were much lower than those of ARRB2 in AD. Thus, our findings indicate that ARRB1/2 play different roles in Aβ25-35 cytotoxicity, which may provide additional support for exploring the underlying molecular mechanism of AD.
format	article
author	Yi-qing Liu Meng-qi Jia Zhao-hong Xie Xiao-fei Liu Hui-Yang Xiao-lei Zheng Hui-qing Yuan Jian-zhong Bi
author_facet	Yi-qing Liu Meng-qi Jia Zhao-hong Xie Xiao-fei Liu Hui-Yang Xiao-lei Zheng Hui-qing Yuan Jian-zhong Bi
author_sort	Yi-qing Liu
title	Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells
title_short	Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells
title_full	Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells
title_fullStr	Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells
title_full_unstemmed	Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells
title_sort	arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nach receptor in sh-sy5y cells
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/67019f06892b4c4e970964bf203f83e3
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Arrestins contribute to amyloid beta-induced cell death via modulation of autophagy and the α7nAch receptor in SH-SY5Y cells

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