Bioinformatics analysis identifies CSF1R as an essential gene mediating Neuropathic pain - Experimental research

Background: Neuropathic pain (NP) severely affects the quality of life; however, there is no effective long-term treatment. The spinal dorsal horn (SDH) is an essential target for studying NP mechanisms and clinical treatments.

Materials and methods: We searched the Gene Expression Omnibus (GEO) for the datasets of SDH microarray changes in mice NP models. Bioinformatics analysis was conducted to identify differentially expressed genes (DEGs), DEG enrichment pathways, and critical hub genes in the datasets. Finally, we explored the expression, function, and relevant mechanisms of the mouse NP model's most critical hub gene.

Results: Two SDH microarray datasets for the mice NP model were retrieved from GEO, GSE75072, and GSE111216. We found 43 overlapping DEGs in the datasets, primarily in the inflammatory and immune pathways. The most essential hub gene was the colony-stimulating factor 1 receptor (CSF1R). Seven days after creating the mouse NP model-spared nerve injury (SNI) model or Sham model, the expression of CSF1R and microglia increased significantly in the SDH of SNI group. PLX3397, an inhibitor of CSF1R, reduced the SDH CSF1R and microglia expression after SNI and significantly alleviated the hyperalgesia in the SNI mice.

Conclusion: SDH CSF1R participates in regulation NP, which is related to changes in the activity of microglia in the SDH.