Exploration of shared gene signatures and molecular mechanisms between psoriasis and COVID-19: evidence from transcriptome data.

IF 2.6 4区 生物学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Rong-Jing Dong, Lu-Hui Yang, Yu-Ye Li, You-Wang Lu
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引用次数: 0

Abstract

Emerging evidence suggests that the onset or worsening of psoriasis can occur following COVID-19 infection or vaccination. Additionally, individuals with psoriasis may be more susceptible to COVID-19. However, the underlying mechanisms driving this phenomenon remain unclear. This study aims to explore the potential shared mechanisms and the complex interplay between psoriasis and COVID-19. Gene expression profiles for COVID-19 (GSE162183) and psoriasis (GSE54456) were obtained from the Gene Expression Omnibus (GEO) database. Common differentially expressed genes (DEGs) were identified, followed by functional annotation, protein–protein interaction (PPI) network construction, and hub gene identification. Validation of hub genes was performed using independent datasets (GSE152075 and GSE157103 for COVID-19; GSE121212 and GSE78097 for psoriasis). Receiver operating characteristic (ROC) curves were used to assess the predictive value of the hub genes. Gene set enrichment analysis (GSEA) and immune infiltration analysis were conducted, and expression patterns of the hub genes were further explored using a single-cell RNA sequencing dataset. A total of 66 common DEGs (all upregulated) were identified. The influenza A and NOD-like receptor signaling pathways were enriched in both COVID-19 and psoriasis. OAS2, MX1, IRF7, RSAD2, OASL, IFIT1, IFIT3, and ISG15 were identified as hub genes after validation, with all are under the curve (AUC) > 0.7 for COVID-19 and AUC > 0.9 for psoriasis. Upregulation of these hub genes was associated with increased infiltration of neutrophils and Th17 cells. Single-cell analysis showed that the hub genes were primarily expressed in epithelial cells in COVID-19 and keratinocytes in psoriasis. This study reveals shared pathogenic mechanisms between psoriasis and COVID-19 and provides insights into how COVID-19 may exacerbate psoriasis. The identified common pathways, hub genes, and associated cell types offer valuable guidance for future research and potential therapeutic targets.

银屑病和COVID-19之间共享基因特征和分子机制的探索:来自转录组数据的证据
新出现的证据表明,牛皮癣的发病或恶化可能发生在COVID-19感染或接种疫苗之后。此外,牛皮癣患者可能更容易感染COVID-19。然而,驱动这一现象的潜在机制尚不清楚。本研究旨在探讨银屑病与COVID-19之间潜在的共同机制和复杂的相互作用。从Gene expression Omnibus (GEO)数据库中获得COVID-19 (GSE162183)和牛皮癣(GSE54456)的基因表达谱。首先鉴定共同差异表达基因(DEGs),然后进行功能注释、蛋白-蛋白相互作用(PPI)网络构建和枢纽基因鉴定。中心基因的验证使用独立的数据集进行(COVID-19的GSE152075和GSE157103;牛皮癣的GSE121212和GSE78097)。采用受试者工作特征(ROC)曲线评估枢纽基因的预测价值。进行了基因集富集分析(GSEA)和免疫浸润分析,并利用单细胞RNA测序数据集进一步探索枢纽基因的表达模式。共鉴定出66个常见的deg(均上调)。甲型流感和nod样受体信号通路在COVID-19和牛皮癣中均富集。经验证,OAS2、MX1、IRF7、RSAD2、OASL、IFIT1、IFIT3和ISG15被确定为枢纽基因,在COVID-19和牛皮癣中AUC均低于曲线(AUC > 0.7和AUC > 0.9)。这些中枢基因的上调与中性粒细胞和Th17细胞的浸润增加有关。单细胞分析显示,hub基因主要表达于2019冠状病毒病的上皮细胞和牛皮癣的角质形成细胞。本研究揭示了银屑病与COVID-19之间的共同致病机制,并为COVID-19如何加剧银屑病提供了见解。已确定的共同途径、枢纽基因和相关细胞类型为未来的研究和潜在的治疗靶点提供了有价值的指导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Mammalian Genome
Mammalian Genome 生物-生化与分子生物学
CiteScore
4.00
自引率
0.00%
发文量
33
审稿时长
6-12 weeks
期刊介绍: Mammalian Genome focuses on the experimental, theoretical and technical aspects of genetics, genomics, epigenetics and systems biology in mouse, human and other mammalian species, with an emphasis on the relationship between genotype and phenotype, elucidation of biological and disease pathways as well as experimental aspects of interventions, therapeutics, and precision medicine. The journal aims to publish high quality original papers that present novel findings in all areas of mammalian genetic research as well as review articles on areas of topical interest. The journal will also feature commentaries and editorials to inform readers of breakthrough discoveries as well as issues of research standards, policies and ethics.
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