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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Global gene expression and chromatin accessibility of the peripheral nervous system in animal models of persistent pain

Fig. 2

Shared DEGs following CCI and CFA in the rat DRG. A Venn diagram shows the number of genes that are differentially expressed after CCI versus naïve (green), CFA versus naïve (orange), or in both models (purple). Log2FC expression of DEGs after CCI (x-axis) and after CFA injection (y-axis). Threshold of |log2FC| > 0.5 (dashed lines) with an FDR < 0.05 designates DEGs after CCI (green), CFA injection (orange), or DEGs found in both models (purple). B Bar plot showing the top 20 GO biological processes significantly enriched in DEGs upregulated (top; green bars) and downregulated (bottom; purple bars) in both the CCI and CFA pain models. C Table which shows the number of DEGs whose gene product is a member of each type of protein. For all common DEGs, the type of each gene product was identified for all DEGs upregulated and downregulated. A greater number of gene encoding GCPRs and Ion channels are upregulated in both models than the number downregulated. The data for these genes are provided in (D) and (E). A lower number of genes encoding transcriptional regulators are upregulated in both pain models than the number downregulated. The data for these genes are provided in (F). DF Heatmaps showing the DEGs that are in common following both CCI and CFA models of chronic pain for genes that encode GCPRs (D), ion channels (E), and transcriptional regulators (F). Colors in each row represent normalized gene counts for a single gene across the 2 biological replicates for each of the naïve, CFA, and CCI groups. CCI chronic constriction injury, CFA complete Freund’s adjuvant, DEG differentially expressed gene, FC fold change, FDR false discovery rate, GO gene ontology

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