POS0743 GENE EXPRESSION MICROARRAY IN LUPUS NEPHRITIS BY BIOINFORMATIC ANALYSIS

Background: Nephritis is one of the predominant causes morbidity and mortality in patients with lupus 1 2 .The lack understanding regarding molecular mechanisms nephritis(LN) hinders development specific targeted therapy for this progressive disease 3 . Objectives: In study, we use bioinformatics method to analyze genes involved regulating potential pathogenesis LN. Methods: The expression profile LN(GSE104948 GSE32591) was obtained from GEO database.GSE104948 a memory chip, which included 32 LN glomerular biopsy tissues living donors.GSE32591 dataset 15 donors. Oligo package used process data obtain matrix files all related genes.P<0.05 |log2(FC)|>2 were setted as cut-off criteria DEGs.Ggplot2, heatmap packages DEGs visualization. Metascape online tool annotating Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment analysis performed.We STRING database construct protein-protein interaction (PPI) network. Hub identified by Cytoscape. Results: differential analysis,357 identified,including 248 up-regulated 109 down-regulated (Figure 1A,B).GO showed that these primarily enriched biological pathways, cell localization function revealed LN-related mainly immune response.KEGG annotation closely associated Staphylococcus aureus infection,Complement coagulation cascades 1D). Fourteen hub genes(IFT3,IRF7,OAS3,GBP2,RSAD2,MX1,IFIT2,IFI6,MX2,ISF15,IFIT1,QAS2,OASL,OAS1) PPI network 1C,E). Conclusion: Illuminating help deep References: [1]Song J, Zhao L, Li Y. Comprehensive mRNA profiles identification miRNA-mRNA nephritis. Lupus 2020;29(8):854-61. doi: 10.1177/0961203320925155 [published Online First: 2020/05/22]. [2]Yao F, Sun Fang W, et al. HsamiR3715p inhibits human mesangial proliferation promotes apoptosis nephritis directly targeting hypoxiainducible factor 1alpha. Mol Med Rep 2016;14(6):5693-98. 10.3892/mmr.2016.5939 2016/11/24]. [3]Dall’Era M. Treatment nephritis: current paradigms emerging strategies. Curr Opin Rheumatol 2017;29(3):241-47. 10.1097/BOR.0000000000000381 2017/02/17]. 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