| 摘要: |
| 通过生物信息学方法分析IFN-γ(Interferon-gamma,干扰素-γ)诱导银屑病皮损的关键基因及可能的作用机制。从GEO(Gene Expression Omnibus)数据库的GPL571平台下载GSE32407 mRNA基因芯片数据集进行基因转录谱分析。设定阈值为|Log2(FC)|(差异表达倍数2倍的绝对值)≥1且P＜0.05,筛选出差异基因。绘制火山图、韦恩图、蛋白质互作网络图、GO(Gene Ontology,基因本体论)/KEGG(Kyoto Encyclopedia of Genes and Genomes,京都基因和基因组百科全书)富集分析图。健康人组和银屑病病人组共筛选出1 321个DEGs(Differentially expressed genes,差异表达基因),PPI(Protein-Protein Interaction,蛋白质互相作用)网络筛选出ISG15、IFIT1、RSAD2、MX1、IFIT3、IFIT2、IRF7、STAT2、MX2、OASL等十个关键作用基因,国内外已有研究对IFIT3、IFIT2、OASL等3个基因与银屑病的关系关注较少,这3个基因可能成为导致银屑病的重要基因,但尚需实验验证。基于本文生信分析的预测结果,推导出IFN-γ可能通过关键基因的表达,促进角质形成细胞增殖、树突状细胞成熟和中性粒细胞浸润,导致局部炎症反应,从而导致银屑病,可为治疗银屑病的靶向药物研究和IFN-γ 诱导银屑病动物模型提供一定的理论依据,但这个推论仅是通过生信分析推导的,因此还需要进一步的实验验证。 |
| 关键词: IFN-γ 银屑病 基因表达差异 作用机制 |
| DOI：10.12113/202207010 |
| 分类号:R758.63 |
| 文献标识码:A |
| 基金项目: |
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| Bioinformatics analysis of key genes and mechanisms of action in IFN-γ induced psoriasis |
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YANG Li1,LI Donghai2
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(1. The First Clinical Medical School of Guangzhou University of Chinese Medicine, Guangzhou 510405,China;2.The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou 510405,China)
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| Abstract: |
| HJ1.00mm]To analyze the key genes and possible mechanisms of action of Interferon-gamma (IFN-γ) induced psoriasis skin lesions by bioinformatics method. GSE32407 mRNA microarray dataset was downloaded from the GPL571 platform of GEO (Gene Expression Omnibus) database for gene transcription profiling. A threshold of | Log2 (FC) | (absolute value of 2-folddifferential expression)≥ 1 and P < 0.05was set to screen out differential genes. Volcano map, Venn map, protein interaction network map and GO (Gene Ontology)/KEGG (Kyoto Encyclopedia of Genes and Genomes) enrichment analysis map were drawn. A total of 1321 DEGs (Differentially expressed genes, differentially expressed genes) and PPI (Protein-Protein Interaction) were screened out in the healthy group and the psoriasis group. Protein interaction network screened out ten key genes including ISG15, IFIT1, RSAD2, MX1, IFIT3, IFIT2, IRF7, STAT2, MX2and OASL.Studies at home and abroad have paid little attention to the relationship between IFIT3, IFIT2and OASLgenes and psoriasis. These three genes may be important pathogenic genes in psoriasis, but need experimental verification. Based on the prediction results of this analysis, it is concluded that IFN-γ may promote keratinocyte proliferation, dendritic cell maturation and neutrophil infiltration through the expression of key genes, leading to local inflammatory response, and thus leading to psoriasis. It provides a theoretical basis for the study of targeted drugs for the treatment of psoriasis and the animal model of IFN-γ induced psoriasis. However, this inference is only derived by means of biogenic analysis, so further experimental verification is needed. |
| Key words: Interferon-gamma Psoriasis Differentially expressed genes Mechanism |
