Isolation and expression profiling of genes upregulated in bone marrow-derived mononuclear cells of rheumatoid arthritis patients
Isolation and expression profiling of genes upregulated in bone marrow-derived mononuclear cells of rheumatoid arthritis patients
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DOI：
10.1093/dnares/dsl006
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发表时间：
2006-08-31
期刊：
影响因子：
4.1
通讯作者：
Ochi, Takahiro
中科院分区：
文献类型：
--
作者：
Nakamura, Nobuo;Shimaoka, Yasunori;Ochi, Takahiro
我们综合鉴定了类风湿性关节炎（RA）患者骨髓源性单核细胞（BMMC）中表达增强的基因与骨关节炎（OA）患者骨髓源性单核细胞（BMMC）中表达增强的基因，并将其命名为AURA。采用逐步减法杂交和微阵列分析鉴定AURA基因，并通过northern blot分析和/或逆转录聚合酶链反应（RT-PCR）证实。我们还通过实时定量RT-PCR评估了它们在个体患者中的表达水平。在我们鉴定的103个AURA基因中，以下10个基因的mRNA水平在许多RA患者中升高，这些基因与免疫反应有关：AREG （=AURA9）、fk506结合蛋白5 （FKBP5 = AURA45）、c型凝集素超家族成员9 （CLECSF9 = AURA24）、酪氨酸蛋白硫转移酶1 （TPST1 = AURA52）、淋巴细胞G0/G1开关基因（G0S2 = AURAS）、趋化因子受体4 （CXCR4 =AURA 86）、核因子κ B （nf - κ B =AURA 25）和两个功能未知的基因（FLJ11106 = AURA1、BC022398 = AURA2、XM_058513 = AURA17）。由于AREG在许多RA患者中显著增加，我们对其进行了进一步分析，发现AREG表皮生长因子受体信号在RA患者分离的滑膜细胞中高度激活，而在OA滑膜细胞中则没有。我们认为这些AURA基因的表达谱可以提高我们对RA发病机制的理解。
We have comprehensively identified the genes whose expressions are augmented in bone marrow-derived mononuclear cells (BMMC) from patients with Rheumatoid Arthritis (RA) as compared with BMMCs from Osteoarthritis (OA) patients, and named them AURA after augmented in RA. Both stepwise subtractive hybridization and microarray analyses were used to identify AURA genes, which were confirmed by northern blot analysis and/or reverse transcription polymerase chain reaction (RT-PCR). We also assessed their expression levels in individual patients by quantitative real-time RT-PCR. Of 103 AURA genes we have identified, the mRNA levels of the following 10 genes, which are somehow related to immune responses, were increased in many of the RA patients: AREG (=AURA9), FK506-binding protein 5 (FKBP5 = AURA45), C-type lectin superfamily member 9 (CLECSF9 = AURA24), tyrosylprotein sulfotransferase 1 (TPST1 = AURA52), lymphocyte G0/G1 switch gene (G0S2 = AURAS), chemokine receptor 4 (CXCR4 = AURA 86), nuclear factor-kappa B (NF-kappa B = AURA 25) and two genes of unknown function (FLJ11106 = AURA1, BC022398 = AURA2 and XM_058513 = AURA17). Since AREG was most significantly increased in many of the RA patients, we subjected it to further analysis and found that AREG-epidermal growth factor receptor signaling is highly activated in synovial cells isolated from RA patients, but not in OA synoviocytes. We propose that the expression profiling of these AURA genes may improve our understanding of the pathogenesis of RA.