Fig. 5.

CRP induces phosphorylation of ERK and Akt, and inhibiting both pathways abrogated the increasing of VEGF production. a, b CRP induced phosphorylation of ERK, Akt, and NF-kB; the effect peaked at 120 min. Pharmacological inhibitors of MAPK (PD98059), PI3K/AKT (LY294002), and NF-ĸB (BAY-11-7082) inhibited the CRP-mediated increase of phosphorylated kinases. LY249002 (10 μM) for PI3K-specific inhibitor, PD98059 (10 μM) for MAPK inhibitor, BAY-11-7082 (10 μM) for inhibitor for NF-ĸB. Inhibitor concentrations were chosen based on the manufacturer’s recommendations and our preliminary experimental findings. c Effects of kinase inhibitors on CRP-induced VEGF production examined by ELISA. Inhibition of the MAPK and PI3K/AKT signaling pathways but not NF-ĸB/IkBα and cycloheximide partly abrogated the increased CRP-induced VEGF production. Columns, mean; bars, SE. *p < 0.05. The results are representative of three independent experiments. CRP C-reactive protein, VEGF vascular endothelial growth factor