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USP13 mediates PTEN to ameliorate osteoarthritis by restraining oxidative stress, apoptosis and inflammation via AKT-dependent manner by Jianming Huang; Zhiyang Ye; Jun Wang; Qichuan Chen; Danlei Huang; Haoyuan Liu is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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Osteoarthritis is a chronic, systemic and inflammatory disease. However, the pathogenesis and understanding of RA are still limited. Ubiquitin-specific protease 13 (USP13) belongs to the deubiquitinating enzyme (DUB) superfamily, and has been implicated in various cellular events. Nevertheless, its potential on RA progression has little to be investigated. In the present study, we found that USP13 expression was markedly up-regulated in synovial tissue samples from patients with RA, and was down-regulated in human fibroblast-like synoviocytes (H-FLSs) stimulated by interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α) or lipopolysaccharide (LPS). We then showed that over-expressing USP13 markedly suppressed inflammatory response, oxidative stress and apoptosis in H-FLSs upon IL-1β or TNF-α challenge, whereas USP13 knockdown exhibited detrimental effects. In addition, USP13-induced protective effects were associated with the improvement of nuclear factor erythroid 2-related factor 2 (Nrf-2) and the repression of Casapse-3. Furthermore, phosphatase and tensin homolog (PTEN) expression was greatly improved by USP13 in H-FLSs upon IL-1β or TNF-α treatment, whereas phosphorylated

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Author

Jianming Huang; Zhiyang Ye; Jun Wang; Qichuan Chen; Danlei Huang; Haoyuan Liu

Publisher

Elsevier Science; Elsevier ; Elsevier Masson; Elsevier BV (ISSN 0753-3322)

Published

2020

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)