β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages

Rheumatoid arthritis (RA) is a chronic inflammatory joint disorder that inflicts damage to the joints of the hands and wrist. The aim of this study was to investigate the protective effect of β-Arrestin-2 (βArr2) on RA in vivo and in vitro. The βArr2 adenovirus (βArr2-Ad) or the control (Con-Ad) was...

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Autores principales:	Feng Cao, Cheng Huang, Jiwei Cheng, Zhaochun He
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	rheumatoid arthritis β-arrestin-2 nf-κb nlrp3 Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/66823c11a7e441a09ce273c3acf4374f
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spelling	oai:doaj.org-article:66823c11a7e441a09ce273c3acf4374f2021-11-26T11:19:49Zβ-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages2165-59792165-598710.1080/21655979.2021.2003678https://doaj.org/article/66823c11a7e441a09ce273c3acf4374f2021-11-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.2003678https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Rheumatoid arthritis (RA) is a chronic inflammatory joint disorder that inflicts damage to the joints of the hands and wrist. The aim of this study was to investigate the protective effect of β-Arrestin-2 (βArr2) on RA in vivo and in vitro. The βArr2 adenovirus (βArr2-Ad) or the control (Con-Ad) was injected into the ankle joint cavity of collagen-induced arthritis (CIA) mice. According to the results, an improvement was shown in the symptoms and pathological injury of RA after an upregulation of βArr2. Correspondingly, the inflammatory response was attenuated, as evidenced by the decreased serum pro-inflammatory cytokines levels and NF-κB pathway-related proteins. Nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor 3 (NLRP3) inflammasome activation was inhibited in CIA mice treated with βArr2-Ad injection, as reflected by the diminished IL-18 level and declined protein levels of ankle inflammasome components in the ankle joint. Likewise, the anti-inflammatory effect of macrophages was also validated by in vitro experiments. In summary, βArr2 effectively ameliorates ankle inflammation in CIA mice via NF-κB/NLRP3 inflammasome, providing theoretical and clinical basis for RA therapy. Key words Rheumatoid arthritis; β-arrestin-2; NF-κB; NLRP3Feng CaoCheng HuangJiwei ChengZhaochun HeTaylor & Francis Grouparticlerheumatoid arthritisβ-arrestin-2nf-κbnlrp3BiotechnologyTP248.13-248.65ENBioengineered, Vol 0, Iss 0 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	rheumatoid arthritis β-arrestin-2 nf-κb nlrp3 Biotechnology TP248.13-248.65
spellingShingle	rheumatoid arthritis β-arrestin-2 nf-κb nlrp3 Biotechnology TP248.13-248.65 Feng Cao Cheng Huang Jiwei Cheng Zhaochun He β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages
description	Rheumatoid arthritis (RA) is a chronic inflammatory joint disorder that inflicts damage to the joints of the hands and wrist. The aim of this study was to investigate the protective effect of β-Arrestin-2 (βArr2) on RA in vivo and in vitro. The βArr2 adenovirus (βArr2-Ad) or the control (Con-Ad) was injected into the ankle joint cavity of collagen-induced arthritis (CIA) mice. According to the results, an improvement was shown in the symptoms and pathological injury of RA after an upregulation of βArr2. Correspondingly, the inflammatory response was attenuated, as evidenced by the decreased serum pro-inflammatory cytokines levels and NF-κB pathway-related proteins. Nucleotide-binding domain leucine-rich repeat and pyrin domain containing receptor 3 (NLRP3) inflammasome activation was inhibited in CIA mice treated with βArr2-Ad injection, as reflected by the diminished IL-18 level and declined protein levels of ankle inflammasome components in the ankle joint. Likewise, the anti-inflammatory effect of macrophages was also validated by in vitro experiments. In summary, βArr2 effectively ameliorates ankle inflammation in CIA mice via NF-κB/NLRP3 inflammasome, providing theoretical and clinical basis for RA therapy. Key words Rheumatoid arthritis; β-arrestin-2; NF-κB; NLRP3
format	article
author	Feng Cao Cheng Huang Jiwei Cheng Zhaochun He
author_facet	Feng Cao Cheng Huang Jiwei Cheng Zhaochun He
author_sort	Feng Cao
title	β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages
title_short	β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages
title_full	β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages
title_fullStr	β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages
title_full_unstemmed	β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages
title_sort	β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing nlrp3 inflammasome activation and nf- κb pathway in macrophages
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/66823c11a7e441a09ce273c3acf4374f
work_keys_str_mv	AT fengcao barrestin2alleviatesrheumatoidarthritisinjurybysuppressingnlrp3inflammasomeactivationandnfkbpathwayinmacrophages AT chenghuang barrestin2alleviatesrheumatoidarthritisinjurybysuppressingnlrp3inflammasomeactivationandnfkbpathwayinmacrophages AT jiweicheng barrestin2alleviatesrheumatoidarthritisinjurybysuppressingnlrp3inflammasomeactivationandnfkbpathwayinmacrophages AT zhaochunhe barrestin2alleviatesrheumatoidarthritisinjurybysuppressingnlrp3inflammasomeactivationandnfkbpathwayinmacrophages
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β-arrestin-2 alleviates rheumatoid arthritis injury by suppressing NLRP3 inflammasome activation and NF- κB pathway in Macrophages

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