Fig. 5

C3aR signaling shifts CAF function via PI3K activation. a Dynamic up-regulation of phosphorylated AKT (Ser473) in CAFs stimulated with rmC3a at different time points. b Dynamic phosphorylated AKT (Ser473) expression of C3aR^−/− CAFs treated with rmC3a at different time points. c rmC3a-induced phosphorylated AKT (Ser473) expression of WT CAFs after pretreatment of C3aR antagonist (SB290157), PI3K inhibitor (LY294002), or C3aR antibodies (14D4). d α-SMA expression of C3a-induced CAFs blocked with C3aR antagonist, PI3K inhibitor, or C3aR antibodies. (*p < 0.05) (e) Transwell assay demonstrated that rmC3a treated CAF facilitate migration capacity of 4 T1 cells, and can be inhibited by C3aR antagonist and PI3K inhibitor. (**p < 0.01,***p < 0.001,****p < 0.0001) (f)TGF-ß1 secretion of CAF stimulated by rmC3a after blockade with C3aR antagonist or PI3K inhibitor (LY294002), compared with medium only. (*p < 0.05)