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首页> 外文期刊>Journal of cellular physiology. >Syndecan-4 involves in the pathogenesis of rheumatoid arthritis by regulating the inflammatory response and apoptosis of fibroblast-like synoviocytes
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Syndecan-4 involves in the pathogenesis of rheumatoid arthritis by regulating the inflammatory response and apoptosis of fibroblast-like synoviocytes

机译：Syndecan-4涉及的发病机理通过规范类风湿性关节炎炎症反应和细胞凋亡呈synoviocytes

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Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease, and the pathogenesis of RA is still unknown. Rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs) are of significance in the pathogenesis of RA. In this study, three microarray profiles (GSE55457, GSE55584, and GSE55235) of human joint FLSs from 33 RA patients and 20 normal controls were extracted from the Gene Expression Omnibus Dataset and analyzed to investigate the underlying pathogenesis of RA. As analyzed by the differently expressed genes, gene ontology, Kyoto Encyclopedia of Genes and Genomes pathway enrichment, and protein-protein interaction network analysis, syndecan-4 (SDC4), a receptor of multiple cytokines and chemokines, which played a key role in the regulation of inflammatory response, was found to be an essential regulator in RA. To further validate these results, the levels of SDC4, reactive oxygen species (ROS), nitric oxide (NO), inflammation, and apoptosis in RA-FLSs were examined. SDC4-silenced RA-FLSs were also used. The results demonstrated that SDC4 and the level of ROS, NO, and inflammation were highly expressed while the apoptosis was decreased in RA-FLSs compared with normal FLSs. SDC4 silencing significantly suppressed the levels of ROS, NO, and inflammation; elevated the expression of nuclear factor erythroid 2-related factor 2; and promoted the apoptosis of RA-FLSs. Collectively, our results demonstrated a new mechanism of SDC4 in initiating the inflammation and inhibiting the apoptosis of RA-FLSs and that a potential target for the diagnosis and treatment of RA in the clinic might be developed.
机译：类风湿性关节炎(RA)是一种慢性自身免疫性炎性疾病,风湿性关节炎的发病机理目前还不清楚。呈synoviocytes (RA-FLSs)意义在RA的发病机制。研究中,三个微阵列资料(GSE55457GSE55584和GSE55235)人类联合fls的33 RA患者和20名正常对照组从基因表达中提取混合数据集和分析探讨潜在的RA的发病机制。不同表达基因,基因本体,《京都议定书》百科全书的基因和基因组途径充实和蛋白质的相互作用网络分析,syndecan-4 (SDC4)受体多种细胞因子和趋化因子在调控中发挥了关键作用炎症反应,是一个被发现监管机构在RA至关重要。这些结果,SDC4的水平,无功氧物种(ROS),一氧化氮(NO),炎症和细胞凋亡在RA-FLSs检查。结果表明,SDC4和水平的ROS,高度和炎症表达在细胞凋亡减少RA-FLSs相比正常的读者。显著抑制活性氧的水平,不,和炎症;核转录因子2红细胞两个相关的因素;促进了RA-FLSs的细胞凋亡。我们的研究结果表明SDC4的新机制在启动和抑制炎症细胞凋亡RA-FLSs和一个潜在的目标RA的诊断和治疗诊所可能发达。

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