AB0005 IDENTIFICATION OF KEY GENES AND PATHWAYS FOR PSORIASIS BASED ON GEO DATABASES BY BIOINFORMATICS ANALYSIS

Background: Psoriasis is an immune-mediated, genetic disease manifesting in the skin or joints both, and also has a strong predisposition autoimmune pathogenic traits 1 . The hallmark of psoriasis sustained inflammation that leads to uncontrolled keratinocyte proliferation dysfunctional differentiation. And it’s chronic relapsing disease, which often necessitates long-term therapy 2 Objectives: To investigate molecular mechanisms find potential gene targets for diagnosis treating psoriasis. Methods: Total 334 expression data patients with research (GSE13355 GSE14905 GSE30999) were obtained from Gene Expression Omnibus database. After preprocessing screening differentially expressed genes (DEGs) by R software. Online toll Metascape 3 was used analyze Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analysis DEGs. Interactions proteins encoded DEGs discovered Protein-protein interaction network (PPI) using STRING online Cytoscape software utilized visualize PPI degree each analyzing topological structure network. Results: A total 611 found be GO revealed up-regulated mostly associated defense response external stimulus while down-regulated metabolism synthesis lipids. KEGG suggested they mainly enriched IL-17 signaling, Toll-like receptor signaling PPAR pathways, Cytokine-cytokine lipid metabolism. In addition, top 9 key (CXCL10, OASL, IFIT1, IFIT3, RSAD2, MX1, OAS1, IFI44 OAS2) identified through Cytoscape. Conclusion: may play essential role development pathogeneses References: [1]Boehncke WH, Schon MP. Psoriasis. Lancet 2015;386(9997):983-94. doi: 10.1016/S0140-6736(14)61909-7 [published First: 2015/05/31]. [2]Zhang YJ, Sun YZ, Gao XH, et al. Integrated bioinformatic pathways plaque Mol Med Rep 2019;20(1):225-35. 10.3892/mmr.2019.10241 2019/05/23]. [3]Zhou Y, Zhou B, Pache L, provides biologist-oriented resource systems-level datasets. Nat Commun 2019;10(1):1523. 10.1038/s41467-019-09234-6 2019/04/05]. Acknowledgements: This project supported National Science Foundation China (82001740), Open Fund Key Laboratory Cellular Physiology (Shanxi Medical University) (KLCP2019) Innovation Plan Postgraduate Education Shanxi Province (2020BY078). Disclosure Interests: None declared