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pmid:36254061

Analysis of differentially expressed genes in individuals with noninfectious uveitis based on data in the gene expression omnibus database.

Dandan Zhang · Ning Zhang · Yan Wang · Qian Zhang · Jiadi Wang · Jing Yao

Medicine · 2022 doi:10.1097/MD.0000000000031082

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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title
Analysis of differentially expressed genes in individuals with noninfectious uveitis based on data in the gene expression omnibus database.
doi
10.1097/MD.0000000000031082
pmid
36254061
authors array · 6 items
[0]
Dandan Zhang
[1]
Ning Zhang
[2]
Yan Wang
[3]
Qian Zhang
[4]
Jiadi Wang
[5]
Jing Yao
journal
Medicine
year
2022
abstract
Noninfectious uveitis (NIU), an intraocular inflammation caused by immune-mediated reactions to eye antigens, is associated with systemic rheumatism and several autoimmune diseases. However, the mechanisms underlying the pathogenesis of uveitis are poorly understood. Therefore, we aimed to identify differentially expressed genes (DEGs) in individuals with NIU and to explore its etiologies using bioinformatics tools. GSE66936 and GSE18781 datasets from the gene expression omnibus (GEO) database were merged and analyzed. Functional enrichment analysis was performed, and protein-protein interaction (PPI) networks were constructed. A total of 89 DEGs were identified. Gene ontology (GO) enrichment analysis identified 21 enriched gene sets. Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis identified four core enriched pathways: antigen processing and expression signaling, natural killer (NK) cell-mediated cytotoxicity signaling, glutathione metabolic signal transduction, and arachidonic acid metabolism pathways. PPI network analysis revealed an active component-target network with 40 nodes and 132 edges, as well as several hub genes, including CD27, LTF, NCR3, SLC4A1, CD69, KLRB1, KIR2DL3, KIR3DL1, and GZMK. The eight potential hub genes may be associated with the risk of developing NIU. NK cell-mediated cytotoxicity signaling might be the key molecular mechanism in the occurrence and development of NIU. Our study provided new insights on NIU, its genetics, molecular pathogenesis and new therapeutic targets.
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The limma package was used to correct the filtered databased on |LogFC|≥1.5 and P < .05, and NIU-related differentially expressed genes were obtained.
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Analysis of GEO chip data identified genetic variations between healthy individuals and patients with uveitis (|LogFC|≥1.5 and P < .05) after batch correction for 89 different genes, including 31 upregulated genes (Table 1) and 58 downregulated genes (Table 2).
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sections[9] "3.1. Identification of DEGs" paragraph 2
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Analysis of GEO chip data identified genetic variations between healthy individuals and patients with uveitis (|LogFC|≥1.5 and P < .05) after batch correction for 89 different genes, including 31 upregulated genes (Table 1) and 58 downregulated genes (Table 2).
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Analysis of GEO chip data identified genetic variations between healthy individuals and patients with uveitis (|LogFC|≥1.5 and P < .05) after batch correction for 89 different genes, including 31 upregulated genes (Table 1) and 58 downregulated genes (Table 2).
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However, the mechanisms underlying the pathogenesis of uveitis are poorly understood. Therefore, we aimed to identify differentially expressed genes (DEGs) in individuals with NIU and to explore its etiologies using bioinformatics tools. GSE66936 and GSE18781 datasets from the gene expression omnibus (GEO) database were merged and analyzed. Functional enrichment analysis was performed, and protein-protein interaction (PPI) networks were constructed. A total of 89 DEGs were identified. Gene ontology (GO) enrichment analysis identified 21 enriched gene sets. Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis identified four core enriched pathways: antigen processing and expression signaling, natural killer (NK) cell-mediated cytotoxicity signaling, glutathione metabolic signal transduction, and arachidonic acid metabolism pathways. 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