Xia Xichun, Yu Hai, Li Yanxiang, Liang Yunting, Li Guangqiang, Huang Fang
Department of Dermatology, Zhuhai People's Hospital (Zhuhai Hospital Affiliated with Jinan University), Jinan University, Zhuhai, 519050, People's Republic of China.
The Biomedical Translational Research Institute, Health Science Center (School of Medicine), Jinan University, Guangzhou, 510632, People's Republic of China.
Clin Cosmet Investig Dermatol. 2023 May 18;16:1287-1301. doi: 10.2147/CCID.S413887. eCollection 2023.
Psoriasis is a systemic inflammatory disease, and the mechanism that links psoriasis to depression is still elusive. Hence, this study aimed to elucidate the potential pathogenesis of psoriasis and depression comorbidity.
The gene expression profiles of psoriasis (GSE34248, GSE78097 and GSE161683) and depression (GSE39653) were downloaded from the Gene Expression Omnibus (GEO) DataSets. Functional annotation, protein-protein interaction (PPI) network and module construction, and hub gene identification and co-expression analysis were performed, following identification of the common differentially expressed genes (DEGs) of psoriasis and depression.
A total of 115 common DEGs (55 up-regulated and 60 down-regulated) were identified between psoriasis and depression. Functional analysis indicated that T cell activation and differentiation were predominantly implicated in the potential pathogenesis of these two diseases. In addition, Th17 cell differentiation and cytokines is closely related to both. Finally, 17 hub genes were screened, including CTLA4, LCK, ITK, IL7R, CD3D, SOCS1, IL4R, PRKCQ, SOCS3, IL23A, PDGFB, PAG1, TGFA, FGFR1, RELN, ITGB5 and TNXB, which re-emphasized the importance of the immune system in psoriasis and depression.
Our study reveals the common pathogenesis of psoriasis and depression. These common pathways and hub genes may apply to a molecular screening tool for depression in psoriasis patients, which could help dermatologists optimize patient management in routine care.
银屑病是一种全身性炎症性疾病,将银屑病与抑郁症联系起来的机制仍不清楚。因此,本研究旨在阐明银屑病与抑郁症共病的潜在发病机制。
从基因表达综合数据库(GEO)下载银屑病(GSE34248、GSE78097和GSE161683)和抑郁症(GSE39653)的基因表达谱。在确定银屑病和抑郁症的共同差异表达基因(DEG)后,进行功能注释、蛋白质-蛋白质相互作用(PPI)网络和模块构建,以及枢纽基因鉴定和共表达分析。
在银屑病和抑郁症之间共鉴定出115个共同的DEG(55个上调和60个下调)。功能分析表明,T细胞活化和分化主要参与这两种疾病的潜在发病机制。此外,Th17细胞分化和细胞因子与两者都密切相关。最后,筛选出17个枢纽基因,包括CTLA4、LCK、ITK、IL7R、CD3D、SOCS1、IL4R、PRKCQ、SOCS3、IL23A、PDGFB、PAG1、TGFA、FGFR1、RELN、ITGB5和TNXB,这再次强调了免疫系统在银屑病和抑郁症中的重要性。
我们的研究揭示了银屑病和抑郁症的共同发病机制。这些共同的途径和枢纽基因可能适用于银屑病患者抑郁症的分子筛查工具,这有助于皮肤科医生在日常护理中优化患者管理。