Fig. 4
CRP stimulation induced RA-associated chromatin dysregulation in monocytes. a Schematic depicting the experimental design for CRP stimulation in vitro. PBMCs of OA patients were co-cultured for 12 h with or without CRP, and then monocytes were sorted and used to generate ATAC-seq and RNAseq libraries. b Barplot showing RAASs before and after CRP stimulation in monocytes. The p value was estimated from paired Student’s t test. **p < 0.01. Error bar represent standard error of the mean (SEM). c Diagrams for the average ATAC-seq signal intensity for C1-C3 peaks of control and CRP stimulation in monocyte. The values of p were calculated for the comparison of the average signals within 10 bp of the peak centres using unpaired t-test. d, f GSEA enrichment plots highlighting RNA-seq signals for proinflammation (d), regulation of OC-differentiation (d), and genes related to RA-associated dysregulation (f) of the running enrichment scores (ES) and positions of gene set members among the rank-ordered list from the GSEA. e, g The barplot shows the gene expression of JAK2 (e), SIGLEC15 (e), and TNFRSF1B (g) in the control and CRP stimulation. The p value was estimated from unpaired Student’s t test. *p < 0.05. CRP, C-reaction protein; OA, osteoarthritis; OC, osteoclast; PBMC, peripheral blood mononuclear cell; CRPstim, CRP stimulation; C3, cluster 3; RAAS, RA-associated ATAC-seq score