To investigate the crosstalk between cartilage and fibroblast-like synoviocytes (FLS) in rheumatoid arthritis (RA), we adopted an in vitro coculture system model of collagen-induced arthritis (CIA) cartilage and CIA FLS monolayer. CIA rat samples of the synovium and femur head were collected for isolation of FLS and coculture system. Cartilages were treated with vehicle (Ctrl group), 10 ng/mL interleukin- (IL-) 1α (IL-1α group), and 10 ng/mL IL-1α plus 10 μM dexamethasone (Dex group) for 3 days before coculture with FLS for further 2 days. After the coculture, FLS were collected to determine the influences of articular cartilage on synoviocytes. Whether the CypB-CD147 signaling pathway is involved in the interactions between cartilage and FLS is assayed. Results showed that IL-1α-stimulated CIA cartilage promoted the proliferation and reduced the apoptosis of FLS. Increased inflammatory cytokines and decreased p57 expression were found in cocultured FLS stimulated by IL-1α-challenged CIA cartilage. Upregulation of NF-κB and I-κB kinase β (IKK-β) and downregulation of the inhibitor of NF-κBα (I-κBα) protein were observed in cocultured FLS. After coculture, significant increases in the expression of cyclophilin B (CypB) and CD147 were observed in CIA cartilage and FLS, respectively. Furthermore, results of immunofluorescence staining showed that the anti-CD147 antibody significantly suppressed p65 nuclear translocation in cocultured FLS stimulated by IL-1α-challenged CIA cartilage. In conclusion, inflammatory effects in the cartilage-FLS coculture system are associated with the CypB-CD147 mediating NF-κB pathway which may further enhance the inflammation in RA.

中文翻译：

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CypB-CD147 信号传导涉及胶原诱导性关节炎中软骨和 FLS 之间的串扰。

为了研究类风湿性关节炎 (RA) 中软骨和成纤维细胞样滑膜细胞 (FLS) 之间的串扰，我们采用了胶原诱导性关节炎 (CIA) 软骨和 CIA FLS 单层的体外共培养系统模型。收集 CIA 大鼠滑膜和股骨头样本用于 FLS 和共培养系统的分离。软骨用载体（Ctrl 组）、10 ng/mL 白介素-（IL-）1 α（IL-1 α组）和 10 ng/mL IL-1 α加 10  μM 地塞米松（Dex 组）3 天，然后与 FLS 共培养 2 天。共培养后，收集 FLS 以确定关节软骨对滑膜细胞的影响。检测 CypB-CD147 信号通路是否参与软骨和 FLS 之间的相互作用。结果表明IL- 1α刺激的CIA软骨促进FLS的增殖并减少其凋亡。在 IL-1 α攻击的 CIA 软骨刺激的共培养 FLS 中发现炎症细胞因子增加和 p57 表达降低。NF-的上调κ B和I- κ乙激酶β（IKK- β）和NF-抑制剂的下调κ乙α在共培养的 FLS 中观察到(I- κ B α ) 蛋白。共培养后，分别在 CIA 软骨和 FLS 中观察到亲环蛋白 B (CypB) 和 CD147 的表达显着增加。此外，免疫荧光染色结果表明，抗 CD147 抗体显着抑制了由 IL- 1α攻击的 CIA 软骨刺激的共培养 FLS 中的 p65 核易位。总之，在软骨-FLS共培养系统抗炎作用与CypB的-CD147调解NF-相关κ乙途径，其可进一步增强在RA中的炎症。