Shared and unique genes and pathways between neuropathic and inflammatory pain assays.

BACKGROUND

Current studies mostly concentrate on behavioral differences and have not yet systematically elucidated the molecular distinctions among various chronic pain models.

METHODS

To identify the similarities and differences in gene expression among mice of three kinds of pain models, i.e., spared nerve injury (SNI) model, chronic constriction injury of the sciatic nerve (CCI) model, and the complete Freund's adjuvant-induced chronic inflammatory pain (CFA) model. The lumbar enlargement segments (L5-L6) were collected. Total mRNA was extracted for RNA sequencing. The differentially expressed genes were analyzed by bioinformatics, including GO analysis, KEGG analysis, and PPI network to explore the functions.

RESULTS

Commonalities and significant variations in gene expression were observed among the three pain models. Compared with Sham, there were 60 shared differential genes among the three models, which were mainly involved in oxidative phosphorylation-related biological process (e.g., mt-Nd1). Compared with CCI, SNI upregulated genes were associated with inflammation response (e.g., Ifi204, Ifi27), while downregulated genes were linked to microtubule-based movement (e.g., Dnah7b, Hcmn1); When compared with SNI, CFA upregulated genes were related to axon development (e. g., Oprm1, Gucy1a2, Syn3), whereas downregulated genes were associated with oxidative phosphorylation (e. g., Rpl41, Rpl21); In contrast to CCI, CFA upregulated genes pertained to axon development (e. g., Zbtb16), while downregulated genes were connected to oxidative phosphorylation (e. g., Cyp3a13).

CONCLUSIONS

The three widely employed chronic pain models exhibit both similarities and distinctions, and genes that vary across all three models may serve as potential targets for chronic pain research.