Fig. 4

EIF3C is a potential target for CFH to play a role in inhibiting FLSs and monocyte function. Monocytes and FLS from RA patients were selected respectively, and cells from each patient were divided into two groups. One group was left untreated, and one group was treated with 5 μg/ml CFH for 6 h. A Volcano plot indicated up-regulated (red dots) and down-regulated (blue dots) genes (P value < 0.05 and |log2FC|> 0.5) by RNA sequencing in CFH-treated versus untreated RA monocytes. EIF3C is indicated. B Volcano plot indicated up-regulated (red dots) and down-regulated (blue dots) genes (P value < 0.05 and |log2FC|> 0.5) by RNA sequencing in CFH-treated versus untreated RA monocytes. EIF3C and EIF3CL are indicated. C We selected the genes upregulated in the CFH-treated monocytes and the genes upregulated in the CFH-treated FLS identified by RNA-sequencing and determined the intersecting proteins. We obtained one gene, namely EIF3C. DEGs: Differentially Expressed Genes. D The boxplot shows the relative expression of EIF3C and EIF3CL. E CFH upregulated the protein expression of EIF3C by using Western blot. F CFH combined with TNF-α upregulated protein expression of EIF3C in both RA FLSs and monocytes by using Western blot. Data are expressed as mean ± SEM (n = 6). *p < 0.05