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首页> 外文期刊>Journal of Cellular Physiology >Downregulation of rheumatoid arthritis-related antigen RA-A47 (HSP47/colligin-2) in chondrocytic cell lines induces apoptosis and cell-surface expression of RA-A47 in association with CD9.
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Downregulation of rheumatoid arthritis-related antigen RA-A47 (HSP47/colligin-2) in chondrocytic cell lines induces apoptosis and cell-surface expression of RA-A47 in association with CD9.

机译：Downregulation的风湿性arthritis-related在chondrocytic抗原RA-A47 (HSP47 / colligin-2)细胞系凋亡和细胞表面表达RA-A47 CD9的协会。

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摘要

Previously, we showed that gene expression of the rheumatoid arthritis-related antigen RA-A47, which is identical to human heat shock protein (HSP)47, was downregulated in chondrocytes by inflammatory cytokines such as TNFalpha. Associated with this phenomenon, RA-A47 appeared on the cell surface concomitant with upregulation of metabolic factors related to cartilage destruction. The upregulation of the metabolic factors could be achieved by downregulation of RA-A47 expression with ra-a47-specific anti-sense oligonucleotide. Here, we show that the enhanced surface expression of RA-A47 on a chondrocytic cell line, HCS-2/8 was also a direct result of RA-A47 downregulation by ra-a47 anti-sense oligonucleotide, independent of the cytokine effects. Moreover, cell-surface expression of CD9, a beta1 integrin-associated transmembrane protein that is involved in cell adhesion and cell motility events, was enhanced in the ra-a47 anti-sense oligonucleotide-treated cells. The CD9 was colocalized with RA-A47 on thecell surface, where it may have affected integrin signaling. Furthermore, Annexin-V binding to the cell surface and the level of a number of apoptosis-related genes including caspase-9 were increased after ra-a47 anti-sense oligonucleotide treatment, suggesting that enhanced surface expression of RA-A47 and CD9 may be initiating apoptosis. Differential screening using a cDNA gene array showed induction of metallothionein-III and chemokine receptor CXCR4 and of factors of the Notch signaling pathway by the anti-sense treatment, but not by TNFalpha. Thus, here we show for the first time an alternative mechanism of inducing apoptosis by downregulating molecular chaperones, independent of the action of TNFalpha. The surface-exposed RA-A47 may induce autoantibodies and inflammatory reactions in autoimmune disease situations such as rheumatoid arthritis.
机译：以前,我们表明,基因的表达风湿性RA-A47 arthritis-related抗原,这是相同的人类热休克蛋白(HSP) 47,在软骨细胞表达下调炎性细胞因子如TNFalpha。与这一现象有关,RA-A47出现了在细胞表面和upregulation相伴软骨代谢因素有关破坏。的差别可以通过对这些因素RA-A47 ra-a47-specific反义表达寡核苷酸。表面的表达RA-A47 chondrocytic细胞系,HCS-2/8也的直接结果通过RA-A47差别RA-A47对这些基因的反义寡核苷酸、独立的细胞因子效果。CD9、beta1 integrin-associated跨膜参与细胞粘附和蛋白质ra-a47细胞运动性活动,加强了反义oligonucleotide-treated细胞。是与RA-A47与细胞表面,它可能影响信号转导。此外,Annexin-V绑定到单元表面和一系列的水平包括caspase-9 apoptosis-related基因增加后ra-a47反义寡核苷酸治疗,建议增强的表面RA-A47和CD9的表达可能会启动细胞凋亡。基因阵列显示诱导metallothionein-III和趋化因子受体CXCR4和Notch信号通路的因素由TNFalpha反义治疗,但不是。因此,这里我们首次展示诱导细胞凋亡的机制表达下调分子陪伴,独立TNFalpha的作用。RA-A47可能诱发自身抗体和炎症在自身免疫性疾病情况下的反应类风湿性关节炎。

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