Isolation and expression profiling of genes upregulated in the peripheral blood cells of systemic lupus erythematosus patients

Isolation and expression profiling of genes upregulated in the peripheral blood cells of systemic lupus erythematosus patients
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DOI:
10.1093/dnares/dsi020
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发表时间:
2005-12-31
期刊:
影响因子:
4.1
通讯作者:
Nojima, Hiroshi
Nojima, Hiroshi
中科院分区:
生物学2区
文献类型:
--
作者:
Ishii, Taeko;Onda, Hiroaki;Nojima, Hiroshi

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我们已经确定了基因的表达增强的系统性红斑狼疮(SLE)患者的血细胞中使用“逐步减法”技术沿着与微阵列分析。采用实时荧光定量逆转录聚合酶链反应(RT-PCR)检测31例SLE患者和30例健康对照者的基因表达水平。我们发现,SLE患者中以下8个基因的转录水平显著升高:干扰素(IFN)-α-诱导蛋白27(IF 127),IFN-α-诱导蛋白IFI-15 K(G1 P2),IFN刺激基因20 kDa(ISG 20),上皮基质相互作用1(EPSTI 1),防御素-α(DEFA 3),双调蛋白(AREG)和两个未知功能的基因(BLAST登录号AL 050290和AY 358224 = SLED 1)。与器官特异性自身免疫性疾病特发性血小板减少性紫癜(ITP)相比,IF 127、G1 P2和SLED 1在SLE中优先上调。相反,AREG和AL 050290在ITP中的表达高于SLE。我们将基因表达的变化与SLE的临床/实验室特征相关联,发现ISG 20、EPSTI 1和SLED 1的表达与淋巴细胞计数显著相关。与IFN相关的基因影响SLE是众所周知的,但是我们在这里报道的其他几个与IFN信号无关的新基因将有助于了解SLE的病理生理学。
We have identified the genes whose expressions are augmented in the blood cells of the patients with systemic lupus erythematosus (SLE) using the 'stepwise subtraction' technique along with microarray analysis. The expression levels of these genes were assessed by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR) in 31 SLE patients and 30 healthy controls. We found that the transcription levels of following eight genes were significantly increased in SLE patients; interferon (IFN)-alpha-inducible protein 27 (IF127), IFN-alpha-inducible protein IFI-15K (G1P2), IFN stimulated gene 20 kDa (ISG20), epithelial stromal interaction 1 (EPSTI1), defensin-alpha (DEFA3), amphiregulin (AREG) and two genes of unknown function (BLAST accession nos AL050290 and AY358224 = SLED1). In comparison with idiopathic thrombocytopenic purpura (ITP), an organ-specific autoimmune disease, IF127, G1P2 and SLED1 were preferentially upregulated in SLE. In contrast, AREG and AL050290 were more highly expressed in ITP than in SLE. We correlated changes in gene expression and clinical/laboratory features of SLE and found that expression of ISG20, EPSTI1 and SLED1 are significantly correlated with lymphocyte counts. Genes linked to IFN are well known to influence SLE, but several other novel genes unrelated to IFN signaling we report here would be useful to understand the pathophysiology of SLE.