Background: Rheumatoid arthritis (RA) is a chronic autoimmune disease without effective treatments. This study explored WNT1 inducible signaling pathway protein 1 (WISP1) as a potential target to prevent RA.

Objectives: This study explored WNT 1 inducible signaling pathway protein 1 (WISP 1) as a potential target to prevent RA.

Methods: Ad-shRNA-WISP1 or NC vector was injected in each ankle of collagen-induced arthritis (CIA) rats. Si-WISP1 or NC vector was transfected to TNF-α-induced fibroblast-like synoviocytes (FLSs). The effects of WISP1 knockdown on levels of pro-inflammatory factors in rats or FLSs were examined by RT-qPCR, ELISA, or western blot. CCK-8, EdU, wound-healing, transwell assays were used to estimate the effects of WISP1 knockdown on TNF-α-induced proliferation, migration, and invasion in FLSs. The NLRP3 inflammasome-related proteins were checked by immunohistochemistry, immunofluorescence assay, or western blot in rats or FLSs.

Results: Administration of WISP1 knockdown declined arthritis scores, alleviated joint damage, and reduced synovial inflammation in CIA rats. WISP1 knockdown restrained TNF-α-induced proliferation, migration, and invasion in FLSs. In CIA rats and TNFα-induced FLSs, WISP1 knockdown reduced the secretion of inflammatory factors and restrained NLRP3 inflammasome activation.

Conclusion: WISP1 knockdown effectively inhibited NLRP3 inflammasome activation and inflammatory factors levels, and bringing a candidate target for treatment of RA.

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Acknowledgements: NIL.

Disclosure of Interests: None declared.