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Updated: Jan 29, 2026
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An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
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Transcriptome Profiling of the Anterior Cingulate Cortex in a CFA-Induced Inflammatory Pain Model Identifies
Guang-Xin Xie1,2,3, Jian-Mei Li4, Bai-Tong Liu2,3,4
1College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China.
Genes
|January 28, 2026
Summary
This study identified fibronectin 1 (Fn1), biglycan (Bgn), and lumican (Lum) as key genes in inflammatory pain, offering potential therapeutic targets for rheumatoid arthritis (RA). These genes are linked to central sensitization and extracellular matrix remodeling in RA.
Area of Science:
- Neuroscience
- Immunology
- Genetics
Background:
- Rheumatoid arthritis (RA) is a chronic autoimmune disease causing joint inflammation and bone destruction.
- The complex pathogenesis of RA is not fully understood, and effective treatments are limited.
Purpose of the Study:
- Identify key genes associated with RA.
- Elucidate the biological significance of these genes using bioinformatics and experimental validation.
Main Methods:
- Analyzed whole-transcriptome data from mice with Complete Freund's Adjuvant (CFA)-induced inflammatory pain.
- Identified differentially expressed genes (DEGs), performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment.
- Constructed a protein-protein interaction (PPI) network and identified hub genes using Random Forest.
- Validated gene expression using quantitative PCR (qPCR).
Main Results:
- Identified 76 DEGs (64 upregulated, 12 downregulated).
- Highlighted fibronectin 1 (Fn1), biglycan (Bgn), and lumican (Lum) as hub genes.
- Enrichment analysis revealed roles in inflammatory responses, extracellular matrix (ECM) remodeling, and TGF-β signaling.
- qPCR confirmed upregulation of Fn1, Bgn, and Lum mRNA in the CFA group.
Conclusions:
- Fn1, Bgn, and Lum show potential roles in central sensitization linked to inflammatory pain.
- These findings offer insights into rheumatoid arthritis pathogenesis and potential therapeutic targets.
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