Study on the molecular mechanisms of bone destruction by rheumatoid synovium by using comprehensive gene expression analysis and multiplex cytokine profiling .

为了阐明类风湿性关节炎（RA）和骨关节炎（OA）患者滑膜破坏骨的分子机制，我们通过综合基因表达分析和多分析物谱分析，分析了类风湿性关节炎（RA）和骨关节炎（OA）患者滑膜组织培养中细胞因子、生长因子、粘附分子、蛋白激酶和转录因子等基因和分子标记的表达谱。类风湿滑膜培养的破骨细胞数量高于OA滑膜培养的。在类风湿滑膜培养中，促炎因子和IL-17F基因表达增加，通路分析显示nf - κ- b和p38 Mark信号通路激活。通过多重细胞因子谱分析证实，培养的类风湿滑膜增加了tnf β和IL-17F的产生。结果表明，RA和OA的滑膜组织培养中促炎和T细胞细胞因子谱不同，这可能是RA关节中破骨细胞过度形成的原因。

To clarify the molecular mechanism(s) of bone destruction by rheumatoid synovium, we analyzed the expression profile of gene and molecular markers including cytokines, growth factors, adhesion molecules, protein kinase, and transcription factors by comprehensive gene expression analysis and multiple analyte profiling in the culture of the synovial tissues derived from patients with rheumatoid arthritis (RA) and osteoarthritis (OA). The higher number of osteoclasts was formed in the culture of rheumatoid synovium compared to the culture of OA synovium. In the culture of rheumatoid synovium, the increased gene expression of proinflammatory cytokines and IL-17F was observed and the pathway analysis showed the activation of NFκ-B and p38 Mark signaling. The increased production of TNFβand IL-17F by the cultured rheumatoid synovium was confirmed using multiplex cytokine profiling. The results indicate that the proinflammatory and T cell cytokine profiles differ in the culture of synovial tissues between RA and OA and this may contribute the excessive formation of osteoclasts in RA joints.