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pmid:34271942
Identification of hub genes in rheumatoid arthritis through an integrated bioinformatics approach.
Rui Wu · Li Long · Qiao Zhou · Jiang Su · Wei Su · Jing Zhu
Journal of orthopaedic surgery and research · 2021 doi:10.1186/s13018-021-02583-3
Paper
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Experiment
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Data
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Analysis
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Execution
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Complete file
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Here, we applied bioinformatics analysis to identify the key genes involved in RA.\nMETHODS: GSE77298 was downloaded from the Gene Expression Omnibus (GEO) database. We used the R software screen the differentially expressed genes (DEGs). Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway were analyzed by using the DAVID online tool. The STRING database was used to analyze the interaction of differentially encoded proteins. PPI interaction network was divided into subnetworks using MCODE algorithm and was analyzed using Cytoscape. Gene set enrichment analysis (GSEA) was performed to identify relevant biological functions. qRT-PCR analysis was also performed to verify the expression of identified hub DEGs.\nRESULTS: A total of 4062 differentially expressed genes were selected, including 1847 upregulated genes and 2215 downregulated genes. In the biological process, DEGs were mainly concentrated in the fields of muscle filament sliding, muscle contraction, intracellular signal transduction, cardiac muscle contraction, signal transduction, and skeletal muscle tissue development. In the cellular components, DEGs were mainly concentrated in the parts of cytosol, Z disk, membrane, extracellular exosome, mitochondrion, and M band. In molecular functions, DEGs were mainly concentrated in protein binding, structural constituent of muscle, actin binding, and actin filament binding. KEGG pathway analysis shows that DEGs mainly focuses on pathways about lysosome, Wnt/β-catenin signaling pathway, and NF-κB signaling pathway. CXCR3, GNB4, and CXCL16 were identified as the core genes that involved in the progression of RA. By qRT-PCR analysis, we found that CXCR3, GNB4, and CXCL16 were significantly upregulated in RA tissue as compared to healthy controls.\nCONCLUSION: In conclusion, DEGs and hub genes identified in the present study help us understand the molecular mechanisms underlying the progression of RA, and provide candidate targets for diagnosis and treatment of RA.", "claims": [{"id": "claim-method", "statement": "Statistical analyses were determined by Student’s t test, and the differences between two groups or more than two groups were detected using ANOVA.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:34271942", "locator": "sections[9] \"Statistical analysis\" paragraph 2", "quote": "Statistical analyses were determined by Student’s t test, and the differences between two groups or more than two groups were detected using ANOVA."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:34271942", "locator": "sections[24] \"notes\" paragraph 1", "quote": "The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": null, "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:34271942"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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