Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes

Rheumatoid arthritis (RA) is a worldwide chronic autoimmune inflammatory disease which is affecting approximately 1% of the total population. It is characterized by abnormal proliferation of fibroblast-like synoviocytes (FLS) and increased production of proinflammatory cytokines. In the current stud...

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Main Authors: Xiao-Bo Luo, Jian-Cheng Xi, Zhen Liu, Yu Long, Li-tao Li, Zhan-Peng Luo, Dao-Hong Liu
Format: Article
Language:English
Published: Wiley 2020-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2020/8295149
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author Xiao-Bo Luo
Jian-Cheng Xi
Zhen Liu
Yu Long
Li-tao Li
Zhan-Peng Luo
Dao-Hong Liu
author_facet Xiao-Bo Luo
Jian-Cheng Xi
Zhen Liu
Yu Long
Li-tao Li
Zhan-Peng Luo
Dao-Hong Liu
author_sort Xiao-Bo Luo
collection DOAJ
description Rheumatoid arthritis (RA) is a worldwide chronic autoimmune inflammatory disease which is affecting approximately 1% of the total population. It is characterized by abnormal proliferation of fibroblast-like synoviocytes (FLS) and increased production of proinflammatory cytokines. In the current study, we were aiming to investigate the role of ubiquitin-specific protease 5 (USP5) in the inflammatory process in RA-FLS. Expression of USP5 was found upregulated in RA-FLS compared with that in osteoarthritis- (OA-) FLS, and IL-1β stimulation increased USP5 expression in a time-dependent manner. Furthermore, we found that USP5 overexpression significantly aggravated proinflammatory cytokine production and related nuclear factor κB (NF-κB) signaling activation. Consistently, silencing of USP5 decreased the release of cytokines and inhibited the activation of NF-κB. In addition, USP5 was found to interact with tumor necrosis factor receptor-associated factor 6 (TRAF6) and remove its K48-linked polyubiquitination chains therefore stabilizing TRAF6. Our data showed that a USP5-positive cell regulates inflammatory processes in RA-FLS and suggested USP5 as a potential target for RA treatment.
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publishDate 2020-01-01
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series Mediators of Inflammation
spelling doaj-art-f2c849775e6d49caa2fdfd8df6a69e372025-08-20T03:25:42ZengWileyMediators of Inflammation0962-93511466-18612020-01-01202010.1155/2020/82951498295149Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like SynoviocytesXiao-Bo Luo0Jian-Cheng Xi1Zhen Liu2Yu Long3Li-tao Li4Zhan-Peng Luo5Dao-Hong Liu6Department of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaDepartment of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaDepartment of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaDepartment of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaDepartment of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaDepartment of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaDepartment of Orthopedic, Eighth Medical Center of PLA General Hospital, Beijing 100091, ChinaRheumatoid arthritis (RA) is a worldwide chronic autoimmune inflammatory disease which is affecting approximately 1% of the total population. It is characterized by abnormal proliferation of fibroblast-like synoviocytes (FLS) and increased production of proinflammatory cytokines. In the current study, we were aiming to investigate the role of ubiquitin-specific protease 5 (USP5) in the inflammatory process in RA-FLS. Expression of USP5 was found upregulated in RA-FLS compared with that in osteoarthritis- (OA-) FLS, and IL-1β stimulation increased USP5 expression in a time-dependent manner. Furthermore, we found that USP5 overexpression significantly aggravated proinflammatory cytokine production and related nuclear factor κB (NF-κB) signaling activation. Consistently, silencing of USP5 decreased the release of cytokines and inhibited the activation of NF-κB. In addition, USP5 was found to interact with tumor necrosis factor receptor-associated factor 6 (TRAF6) and remove its K48-linked polyubiquitination chains therefore stabilizing TRAF6. Our data showed that a USP5-positive cell regulates inflammatory processes in RA-FLS and suggested USP5 as a potential target for RA treatment.http://dx.doi.org/10.1155/2020/8295149
spellingShingle Xiao-Bo Luo
Jian-Cheng Xi
Zhen Liu
Yu Long
Li-tao Li
Zhan-Peng Luo
Dao-Hong Liu
Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
Mediators of Inflammation
title Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_full Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_fullStr Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_full_unstemmed Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_short Proinflammatory Effects of Ubiquitin-Specific Protease 5 (USP5) in Rheumatoid Arthritis Fibroblast-Like Synoviocytes
title_sort proinflammatory effects of ubiquitin specific protease 5 usp5 in rheumatoid arthritis fibroblast like synoviocytes
url http://dx.doi.org/10.1155/2020/8295149
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