Ruschpler Peter, Lorenz Peter, Eichler Wolfram, Koczan Dirk, Hänel Claudia, Scholz Roger, Melzer Christian, Thiesen Hans-Jürgen, Stiehl Peter
Institute of Pathology, University of Leipzig, Leipzig, Germany.
Arthritis Res Ther. 2003;5(5):R241-52. doi: 10.1186/ar783. Epub 2003 Jun 26.
To improve our knowledge on the pathophysiology of rheumatoid arthritis (RA), we investigated gene expression patterns in synovial tissue from RA and osteoarthritis (OA) patients. DNA oligonucleotide microarray analysis was employed to identify differentially expressed genes in synovial tissue from pathologically classified tissue samples from RA (n = 20) and OA patients (n = 10). From 7131 gene sets displayed on the microarray chip, 101 genes were found to be upregulated and 300 genes to be downregulated in RA as compared with OA. Semiquantitative reverse-transcription polymerase chain reaction, Western blotting and immunohistochemistry were used to validate microarray expression levels. These experiments revealed that Cys-X-Cys receptor (CXCR)1, CXCR2 and CXCR3 mRNAs, as well as Cys-X-Cys ligand (CXCL)9 (monokine induced by IFN-gamma) and CXCL10 (IFN-gamma inducible protein 10) mRNAs, were significantly upregulated in RA as compared with OA disease. Elevated protein levels in RA synovial tissue were detected for CXCR1 and CXCR3 by Western blotting. Using immunohistochemistry, CXCR3 protein was found to be preferentially expressed on mast cells within synovial tissue from RA patients. These findings suggest that substantial expression of CXCR3 protein on mast cells within synovial tissue from RA patients plays a significant role in the pathophysiology of RA, accompanied by elevated levels of the chemokines CXCL9 and CXCL10. Mature mast cells are likely to contribute to and sustain the inflamed state in arthritic lesions (e.g. by production of inflammatory mediators such as histamine, proteinases, arachidonic acid metabolites and cytokines). Thus, the mast cell could become a potential target in therapeutic intervention.
为了增进我们对类风湿关节炎(RA)病理生理学的了解,我们研究了RA患者和骨关节炎(OA)患者滑膜组织中的基因表达模式。采用DNA寡核苷酸微阵列分析来鉴定RA患者(n = 20)和OA患者(n = 10)经病理分类的组织样本滑膜组织中差异表达的基因。与OA相比,在微阵列芯片上显示的7131个基因集中,发现RA中有101个基因上调,300个基因下调。使用半定量逆转录聚合酶链反应、蛋白质印迹法和免疫组织化学来验证微阵列表达水平。这些实验表明,与OA疾病相比,RA中Cys-X-Cys受体(CXCR)1、CXCR2和CXCR3 mRNA以及Cys-X-Cys配体(CXCL)9(γ干扰素诱导的单核因子)和CXCL10(γ干扰素诱导蛋白10)mRNA显著上调。通过蛋白质印迹法检测到RA滑膜组织中CXCR1和CXCR3的蛋白质水平升高。使用免疫组织化学方法,发现CXCR3蛋白在RA患者滑膜组织内的肥大细胞上优先表达。这些发现表明,RA患者滑膜组织内肥大细胞上CXCR3蛋白的大量表达在RA的病理生理学中起重要作用,同时伴有趋化因子CXCL9和CXCL10水平升高。成熟的肥大细胞可能有助于并维持关节炎病变中的炎症状态(例如通过产生组胺、蛋白酶、花生四烯酸代谢产物和细胞因子等炎症介质)。因此,肥大细胞可能成为治疗干预的潜在靶点。
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