microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3

Qi-Bin Yang,1,2 Ling-Qin Li,1 Quan-Bo Zhang,2,3 Yong-Long He,1 Qing-Sheng Mi,2 Jing-Guo Zhou4 1Department of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 2Henry Ford Immunology Program, De...

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Autores principales:	Yang QB, Li LQ, Zhang QB, He YL, Mi QS, Zhou JG
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2021
Materias:	mir-223 gout animal models cytokines monosodium urate Pathology RB1-214 Therapeutics. Pharmacology RM1-950
Acceso en línea:	https://doaj.org/article/dcb51621b4e0432896168b7a88c94b79
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spelling	oai:doaj.org-article:dcb51621b4e0432896168b7a88c94b792021-12-02T17:02:14ZmicroRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP31178-7031https://doaj.org/article/dcb51621b4e0432896168b7a88c94b792021-05-01T00:00:00Zhttps://www.dovepress.com/microrna-223-deficiency-exacerbates-acute-inflammatory-response-to-mon-peer-reviewed-fulltext-article-JIRhttps://doaj.org/toc/1178-7031Qi-Bin Yang,1,2 Ling-Qin Li,1 Quan-Bo Zhang,2,3 Yong-Long He,1 Qing-Sheng Mi,2 Jing-Guo Zhou4 1Department of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 2Henry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, Detroit, MI, 48202, USA; 3Department of Gerontology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 4Department of Rheumatology and Immunology, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, Sichuan Province, People’s Republic of ChinaCorrespondence: Qing-Sheng MiHenry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, 1 Ford Place, Detroit, MI, 48202, USATel +1-313-876-1017Email qmi1@hfhs.orgJing-Guo ZhouDepartment of Rheumatology and Immunology, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, Sichuan Province, People’s Republic of ChinaTel +86-28-8301-6078Email jgzhou@cmc.edu.cnObjective: MicroRNAs were identified as master-switch molecules limiting acute inflammatory response. This study investigated the potential role of microRNA (miR)-223 in the mechanism of gout.Methods: Wild-type (WT) and miR-223 knock-out (KO) mice were used to evaluate the phenotypes of gout models. Inflammatory cytokines were measured in air pouch and peritoneal cavity lavage fluid. In addition to miR-223 level in gout patients, miR-223 and pro-inflammatory genes were examined in bone marrow-derived macrophages (BMDMs) from mice as well as peripheral blood mononuclear cells from healthy controls (HC) treated with monosodium urate (MSU) crystals in vitro.Results: MiR-223 was up-regulated in the early phase in BMDMs from WT mice after MSU challenge and decreased rapidly, and this was not observed in miR-223 KO mice in vitro. In addition, miR-223 was required for macrophages homeostasis. In comparison with WT mice in vivo, miR-223 deficiency exacerbated swelling index of MSU-induced inflammation in foot pad and ankle joint models. MiR-223 deficiency also markedly aggravated inflammatory cells infiltration and cytokines release including interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) in the air pouch and peritonitis models. In the in vitro experiments, miR-223 deficiency promoted the inflammatory response by targeting NLR family pyrin domain containing protein 3 (NLRP3). Besides, miR-223 level was down-regulated in gout patients and in HC exposed to MSU in vitro.Conclusion: MiR-223 was down-regulated in gout patients and miR-223 deficiency exacerbated inflammatory response in diverse murine models, suggesting that up-regulation of miR-223 could be a potential therapeutic strategy for alleviating gouty inflammation.Keywords: miR-223, gout, animal models, cytokines, monosodium urateYang QBLi LQZhang QBHe YLMi QSZhou JGDove Medical Pressarticlemir-223goutanimal modelscytokinesmonosodium uratePathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 14, Pp 1845-1858 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	mir-223 gout animal models cytokines monosodium urate Pathology RB1-214 Therapeutics. Pharmacology RM1-950
spellingShingle	mir-223 gout animal models cytokines monosodium urate Pathology RB1-214 Therapeutics. Pharmacology RM1-950 Yang QB Li LQ Zhang QB He YL Mi QS Zhou JG microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3
description	Qi-Bin Yang,1,2 Ling-Qin Li,1 Quan-Bo Zhang,2,3 Yong-Long He,1 Qing-Sheng Mi,2 Jing-Guo Zhou4 1Department of Rheumatology and Immunology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 2Henry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, Detroit, MI, 48202, USA; 3Department of Gerontology, Affiliated Hospital of North Sichuan Medical College, Nanchong, 637000, Sichuan Province, People’s Republic of China; 4Department of Rheumatology and Immunology, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, Sichuan Province, People’s Republic of ChinaCorrespondence: Qing-Sheng MiHenry Ford Immunology Program, Departments of Dermatology and Internal Medicine, Henry Ford Health System, 1 Ford Place, Detroit, MI, 48202, USATel +1-313-876-1017Email qmi1@hfhs.orgJing-Guo ZhouDepartment of Rheumatology and Immunology, Clinical Medical College and the First Affiliated Hospital of Chengdu Medical College, Chengdu, 610500, Sichuan Province, People’s Republic of ChinaTel +86-28-8301-6078Email jgzhou@cmc.edu.cnObjective: MicroRNAs were identified as master-switch molecules limiting acute inflammatory response. This study investigated the potential role of microRNA (miR)-223 in the mechanism of gout.Methods: Wild-type (WT) and miR-223 knock-out (KO) mice were used to evaluate the phenotypes of gout models. Inflammatory cytokines were measured in air pouch and peritoneal cavity lavage fluid. In addition to miR-223 level in gout patients, miR-223 and pro-inflammatory genes were examined in bone marrow-derived macrophages (BMDMs) from mice as well as peripheral blood mononuclear cells from healthy controls (HC) treated with monosodium urate (MSU) crystals in vitro.Results: MiR-223 was up-regulated in the early phase in BMDMs from WT mice after MSU challenge and decreased rapidly, and this was not observed in miR-223 KO mice in vitro. In addition, miR-223 was required for macrophages homeostasis. In comparison with WT mice in vivo, miR-223 deficiency exacerbated swelling index of MSU-induced inflammation in foot pad and ankle joint models. MiR-223 deficiency also markedly aggravated inflammatory cells infiltration and cytokines release including interleukin (IL)-1β, IL-6 and monocyte chemotactic protein-1 (MCP-1) in the air pouch and peritonitis models. In the in vitro experiments, miR-223 deficiency promoted the inflammatory response by targeting NLR family pyrin domain containing protein 3 (NLRP3). Besides, miR-223 level was down-regulated in gout patients and in HC exposed to MSU in vitro.Conclusion: MiR-223 was down-regulated in gout patients and miR-223 deficiency exacerbated inflammatory response in diverse murine models, suggesting that up-regulation of miR-223 could be a potential therapeutic strategy for alleviating gouty inflammation.Keywords: miR-223, gout, animal models, cytokines, monosodium urate
format	article
author	Yang QB Li LQ Zhang QB He YL Mi QS Zhou JG
author_facet	Yang QB Li LQ Zhang QB He YL Mi QS Zhou JG
author_sort	Yang QB
title	microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3
title_short	microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3
title_full	microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3
title_fullStr	microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3
title_full_unstemmed	microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3
title_sort	microrna-223 deficiency exacerbates acute inflammatory response to monosodium urate crystals by targeting nlrp3
publisher	Dove Medical Press
publishDate	2021
url	https://doaj.org/article/dcb51621b4e0432896168b7a88c94b79
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microRNA-223 Deficiency Exacerbates Acute Inflammatory Response to Monosodium Urate Crystals by Targeting NLRP3

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