ObjectiveTo investigate key differentially expressed genes (DEGs) in peripheral blood of idiopathic epilepsy patients, as well as their biological functions, cellular localization, involved signaling pathways, through bioinformatics analysis. So to provide new insights for the pathogenesis and prevention of idiopathic epilepsy.MethodsFirstly, we screened and downloaded microarray data including 6 peripheral blood samples of drug-naive patients with idiopathic epilepsy, 8 peripheral blood samples of responders of idiopathic epilepsy treated with Valproate (VPA), and 10 peripheral blood samples of non-responders of idiopathic epilepsy treated with VPA from Gene Expression Omnibus (GEO) data series GSE143272, which Public in January 2020. Secondly, we identified DEGs via the limma package and others in R software. Then we had gotten 74 DEGs, and subsequently conducted gene ontology and pathway enrichment analysis, PPI network analysis and hub gene analysis, using multiple methods containing DAVID, STRING, and Cytohubba in Cytoscape.ResultsWe had identified significant hub DEGs, including TREML3P, KCNJ15, ORM1, RNA28S5, ELANE, RETN, ARG1, LCN2, SLPI, HP, PGLYRP1, BPI, DEFA4, TCN1, MPO, MMP9, CTSG, CXCL8, RNASE3, RNASE2, S100A12, DEFA1B, DEFA1, DEFA3, CEACAM8, MS4A3, PTGS2, PI3, CCL3. The biological processes involved in these DEGs include immune response, inflammatory response, chemotaxis, etc. While, the molecular function is focused on peroxidase activity, chemokine activity, etc. Moreover, KEGG pathway enrichment analysis shows that DEGs were mainly involved in cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway, chemokine signaling pathway and so on.ConclusionThese important key DEGs may be involved in the onset and development of idiopathic epilepsy through a variety of signaling pathways and complex mechanisms.
Objective To explore the pathogenesis of acute respiratory disease syndrome (ARDS) by bioinformatics analysis of neutrophil gene expression profile in order to find new therapeutic targets. Methods The gene expression chips include ARDS patients and healthy volunteers were screened from the Gene Expression Omnibus (GEO) database. The differentially expressed genes were carried out through GEO2R, OmicsBean, STRING, and Cytoscape, then enrichment analysis of Gene Ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) pathways was conducted to investigate the biological processes involved in ARDS via DAVID website. Results Bioinformatics analysis showed 86 differential genes achieved through the GEO2R website. Eighty-one genes were included in the STRING website for protein interaction analysis. The results of the interaction were further analyzed by Cytoscape software to obtain 11 hub genes: AHSP, ALAS2, CD177, CLEC4D, EPB42, GPR84, HBD, HVCN1, KLF1, SLC4A1, and STOM. GO analysis showed that the differential gene was enriched in the cellular component, especially the integrity of the plasma membrane. KEGG analysis showed that multiple pathways especially the cytokine receptor pathway involved in the pathogenesis of ARDS. Conclusions A variety of genes and pathways have been involved in the pathogenesis of ARDS. Eleven hub genes are screened, which may be involved in the pathogenesis of ARDS and can be used in subsequent studies.
Objective To explore the potential mechanism of the occurrence and development of lupus nephritis (LN) and identify key biomarkers and immune-related pathways associated with the progression of LN. Methods We downloaded a dataset from the Gene Expression Omnibus database. By analyzing the differential expression of genes and performing weighted gene co-expression network analysis (WGCNA), as well as Gene Ontology enrichment, Disease Ontology enrichment, and Kyoto Encyclopedia of Genes and Genomes pathway enrichment, we explored the biological functions of differentially expressed genes in LN. Using three machine learning models, namely LASSO regression, support vector machine, and random forest, we identified the hub genes in LN, and constructed a line diagram diagnosis model based on the hub genes. The diagnostic accuracies of the hub genes were evaluated using the receiver operating characteristic curve, and the relationship between known marker gene sets and hub gene expression was analyzed using single sample gene set enrichment analysis. Results We identified a total of 2297 differentially expressed genes. WGCNA generated 7 co-expression modules, among which the cyan module had the highest correlation with LN. We obtained 347 target genes by combining differential genes. Using the three machine learning methods, LASSO regression, support vector machine, and random forest, we identified three hub genes (CLC, ADGRE4P, and CISD2) that could serve as potential biomarkers for LN. The area under the receiver operating characteristic curve (AUC) analysis showed that these three hub genes had significant diagnostic value (AUCCLC=0.718, AUCADGRE4P=0.813, AUCCISD2=0.718). According to single sample gene set enrichment analysis, the hub genes were mainly associated with apoptosis, glycolysis, metabolism, hypoxia, and tumor necrosis factor-α-nuclear factor-κB-related pathways. Conclusions By combining WGCNA and machine learning techniques, three hub genes (CLC, ADGRE4P, and CISD2) that may be involved in the occurrence and development of LN are identified. These genes have the potential to aid in the early clinical diagnosis of LN and provide insight into the mechanisms underlying LN progression.