Figure 5
Cell annotation, marker gene feature plots, and endocannabinoid signaling pathway from neurons of PAG region cells in CFA-induced chronic inflammatory pain model with ApAP and SRP-001 treatments. (a) Heatmap of top 40 canonical pathways for neuronal clusters across samples – CFA_Veh, CFA_ApAP, and CFA_SRP-001 with the comparisons between them as follows – Vehicle vs CFA_Vehicle, CFA_Vehicle vs CFA_ApAP, and CFA_ApAP vs CFA_SRP-001. The heatmap shows that when CFA_Vehicle is compared to Vehicle, there is upregulation of several genes that are predicted to affect cellular signaling related to these pathways highlighted in the heatmap, and when CFA_ApAP and CFA_SRP-001 are compared to CFA_Vehicle, there is downregulation of those upregulated pathways in both cases, with more downregulation for CFA_SRP-001 than CFA_ApAP. (b,c) CellChat computed cell–cell interaction network for CFA_ApAP and CFA_SRP-001 group datasets showing number and strength of interactions describing similarities between the two groups. (d,e) Outgoing communication patterns in individual secreting cell types for CFA_ApAP and CFA_SRP-001. (f) Heatmap of DESeq2-normalized expression values from scRNA-seq data for genes involved in endocannabinoid signaling genes. (g) Endocannabinoid signaling pathways generated by Qiagen Ingenuity Pathway Analysis (IPA) with an overlay based on DESeq2-normalized expression values of differentially expressed genes (DEGs) in neuronal clusters CFA_Vehicle vs CFA_SRP-001 treatments, respectively.
