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Войти в исследования Frontiers in cell and developmental biology · 2026
Granzyme B knockdown suppresses cell proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis.
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Zhang Wei, Tian Weike, Zhang Chao
Аннотация
BACKGROUND: Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by progressive synovial inflammation, cartilage and bone destruction. Although granzyme B (GZMB) can prevent osteocartilaginous destruction and promote bone formation, its effects and molecular mechanisms in RA remain unclear. We therefore explored the effects of GZMB on RA development at the cellular level.
METHODS: We analyzed the effects of GZMB on MH7A cell proliferation using Cell Counting Kit-8 assays. Migration and invasion were detected using wound healing and Transwell® assays, respectively, and the cell cycle and apoptosis were assessed using flow cytometry. Additionally, 24 Sprague-Dawley (SD) rats were divided into sham, RA, and RA + GZMB inhibitor groups. Pathological changes, inflammatory factors, and related proteins were assessed in each group after treatment. Furthermore, we evaluated correlations between GZMB and the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.
RESULTS: Granzyme B suppressed cell proliferation, migration and invasion in vitro, promoted apoptosis, and increased the proportion of cells in the S and G2 phases. Additionally, histological staining revealed that after GZMB inhibitor treatment, the articular cartilage surface of rats in the GZMB inhibitor group was smooth, and synovial tissue hyperplasia and inflammatory cell infiltration were reduced. Moreover, GZMB regulated expression of the PI3K/AKT signaling pathway during RA treatment in vitro and in vivo.
CONCLUSION: Our findings suggest that GZMB knockdown suppresses cell proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis, and alleviates the progression of RA rats. This therapeutic mechanism may involve regulation of the PI3K/AKT pathway.
METHODS: We analyzed the effects of GZMB on MH7A cell proliferation using Cell Counting Kit-8 assays. Migration and invasion were detected using wound healing and Transwell® assays, respectively, and the cell cycle and apoptosis were assessed using flow cytometry. Additionally, 24 Sprague-Dawley (SD) rats were divided into sham, RA, and RA + GZMB inhibitor groups. Pathological changes, inflammatory factors, and related proteins were assessed in each group after treatment. Furthermore, we evaluated correlations between GZMB and the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) pathway.
RESULTS: Granzyme B suppressed cell proliferation, migration and invasion in vitro, promoted apoptosis, and increased the proportion of cells in the S and G2 phases. Additionally, histological staining revealed that after GZMB inhibitor treatment, the articular cartilage surface of rats in the GZMB inhibitor group was smooth, and synovial tissue hyperplasia and inflammatory cell infiltration were reduced. Moreover, GZMB regulated expression of the PI3K/AKT signaling pathway during RA treatment in vitro and in vivo.
CONCLUSION: Our findings suggest that GZMB knockdown suppresses cell proliferation, migration and invasion of fibroblast-like synoviocytes in rheumatoid arthritis, and alleviates the progression of RA rats. This therapeutic mechanism may involve regulation of the PI3K/AKT pathway.