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<p>Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation of the synovial tissue, leading to joint destruction and significant impairment of quality of life. This study aims to elucidate the role of the Budding Uninhibited By Benzimidazoles 1 (BUB1) in the pathogenesis of RA, particularly its expression and regulatory mechanisms in RA synovial fibroblasts. We analyzed BUB1 expression in RA synovial tissues using GEO datasets and western blot was used to validate the expression in TNF-α/IL-1β-stimulated synovial fibroblasts. MTT and colony formation was used to assess the cell proliferation, and traswell assay was used to test the migration of MH7A cells. The expression of IL-6 and IL-1β was tested by ELISA and the key proteins was tested by western blotting in p38/ATF-2 signaling pathway. The results showed that BUB1 knockdown significantly inhibited cell proliferation, migration, and invasion of MH7A cells, coinciding with a marked decrease in the expression of inflammatory cytokines (IL-6, IL-1β), as well as MMP-1 and MMP-9. Furthermore, BUB1 knockdown decreased p38 phosphorylation and ATF-2 activation. In conclusion, BUB1 knockdown reduces inflammatory cytokine and MMP expression in synovial fibroblasts, accompanied by decreased p38/ATF-2 pathway activation. These findings suggest that BUB1 may contribute to RA-associated inflammation and joint destruction, potentially through modulation of the p38/ATF-2 signaling pathway, highlighting BUB1 as a candidate therapeutic target for RA treatment.Key words: BUB1, rheumatoid arthritis, inflammatory, MMPs, p38 pathway.</p>

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BUB1 modulates inflammatory and destructive phenotypes in rheumatoid arthritis synovial fibroblasts via the p38/ATF-2 signaling pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月7日

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  • Hang Zhong,
  • Xin He,
  • Wanquan Cao,
  • Zhaonan Ban

摘要

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent inflammation of the synovial tissue, leading to joint destruction and significant impairment of quality of life. This study aims to elucidate the role of the Budding Uninhibited By Benzimidazoles 1 (BUB1) in the pathogenesis of RA, particularly its expression and regulatory mechanisms in RA synovial fibroblasts. We analyzed BUB1 expression in RA synovial tissues using GEO datasets and western blot was used to validate the expression in TNF-α/IL-1β-stimulated synovial fibroblasts. MTT and colony formation was used to assess the cell proliferation, and traswell assay was used to test the migration of MH7A cells. The expression of IL-6 and IL-1β was tested by ELISA and the key proteins was tested by western blotting in p38/ATF-2 signaling pathway. The results showed that BUB1 knockdown significantly inhibited cell proliferation, migration, and invasion of MH7A cells, coinciding with a marked decrease in the expression of inflammatory cytokines (IL-6, IL-1β), as well as MMP-1 and MMP-9. Furthermore, BUB1 knockdown decreased p38 phosphorylation and ATF-2 activation. In conclusion, BUB1 knockdown reduces inflammatory cytokine and MMP expression in synovial fibroblasts, accompanied by decreased p38/ATF-2 pathway activation. These findings suggest that BUB1 may contribute to RA-associated inflammation and joint destruction, potentially through modulation of the p38/ATF-2 signaling pathway, highlighting BUB1 as a candidate therapeutic target for RA treatment.Key words: BUB1, rheumatoid arthritis, inflammatory, MMPs, p38 pathway.