Open Access

ORIGINAL ARTICLE

NLRP12 reduces proliferation and inflammation of rheumatoid arthritis fibroblast-like synoviocytes by regulating the NF-kB and MAPK pathways

Xin Zhang¹, He Nan¹, Jialong Guo¹, Jinyu Liu²

1 Department of Rheumatology and Immunology, China-Japan Union Hospital of Jilin University, Changchun City, Jilin Province, 130033, China
2 Department of Gynecologyic Oncosurgery-3, Ji Lin Tumor Hospital, Changchun City, Jilin Province, 130031, China

* Corresponding Authors: J. Liu, ; J. Guo,

European Cytokine Network 2021, 32(2), 15-22. https://doi.org/10.1684/ecn.2021.0465

Abstract

Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease characterized by abnormal synovial hyperplasia and the release of inflammatory cytokines. NLRP12 is a member of the family nod-like receptor (NLR) families that are activators of inflammation. However, the role of NLRP12 in fibroblast-like synoviocytes (FLSs) is still unclear. In the present study, we have investigated the role of NLRP12 in fibroblast-like synoviocytes (FLSs). The results demonstrated that NLRP12 overexpression inhibited proliferation and promoted cell apoptosis in RA-FLSs. Moreover, NLRP12 overexpression repressed inflammation by downregulation of IL-1β, TNF-α, IL-6, IFN-γ and MCP-1 production and upregulation of IL-10 levels, with knockdown of NLRP12 expression showing opposite effects. In addition, NLRP12 overexpression suppressed phosphorylation of JNK, ERK, p38 and NF-κB in RA-FLSs, whereas NLRP12 knockdown promoted phosphorylation of these proteins. In conclusion, these findings demonstrate that NLRP12 inhibits proliferation and inflammation of RA-FLSs via the regulation of the NF-κB and MAPK signaling pathways, suggesting that NLRP12 might be a potential target for RA treatment.

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