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Deciphering psoriasis. A bioinformatic approach

机译:解密牛皮癣。 生物信息化方法

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Abstract Background Psoriasis is an immune-mediated, inflammatory and hyperproliferative disease of the skin and joints. The cause of psoriasis is still unknown. The fundamental feature of the disease is the hyperproliferation of keratinocytes and the recruitment of cells from the immune system in the region of the affected skin, which leads to deregulation of many well-known gene expressions. Objective Based on data mining and bioinformatic scripting, here we show a new dimension of the effect of psoriasis at the genomic level. Methods Using our own pipeline of scripts in Perl and MySql and based on the freely available NCBI Gene Expression Omnibus (GEO) database: DataSet Record GDS4602 (Series GSE13355), we explore the extent of the effect of psoriasis on gene expression in the affected tissue. Results We give greater insight into the effects of psoriasis on the up-regulation of some genes in the cell cycle (CCNB1, CCNA2, CCNE2, CDK1) or the dynamin system (GBPs, MXs, MFN1), as well as the down-regulation of typical antioxidant genes (catalase, CAT; superoxide dismutases, SOD1-3; and glutathione reductase, GSR). We also provide a complete list of the human genes and how they respond in a state of psoriasis. Conclusion Our results show that psoriasis affects all chromosomes and many biological functions. If we further consider the stable and mitotically inheritable character of the psoriasis phenotype, and the influence of environmental factors, then it seems that psoriasis has an epigenetic origin. This fit well with the strong hereditary character of the disease as well as its complex genetic background.
机译:摘要背景银屑病是一种免疫介导的皮肤和关节炎性增生性疾病。银屑病的病因尚不清楚。该病的基本特征是角质形成细胞的过度增殖和受影响皮肤区域免疫系统中的细胞募集,这导致许多已知基因表达的去调控。目的基于数据挖掘和生物信息学脚本,我们在基因组水平上展示了银屑病影响的一个新维度。方法使用我们自己的Perl和MySql脚本管道,基于免费提供的NCBI基因表达综合数据库:数据集记录GDS4602(GSE13355系列),我们探索银屑病对受影响组织中基因表达的影响程度。结果我们更深入地了解了银屑病对细胞周期(CCNB1、CCNA2、CCNE2、CDK1)或动态蛋白系统(GBPs、MXs、MFN1)中某些基因上调的影响,以及对典型抗氧化基因(过氧化氢酶、CAT、超氧化物歧化酶、SOD1-3和谷胱甘肽还原酶、GSR)下调的影响。我们还提供了人类基因的完整列表,以及它们在银屑病状态下的反应。结论银屑病影响所有染色体和多种生物学功能。如果我们进一步考虑银屑病表型的稳定和有丝分裂遗传特征,以及环境因素的影响,那么银屑病似乎具有表观遗传起源。这与该病强烈的遗传特征及其复杂的遗传背景非常吻合。

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