Role of JNK and NF-κB pathways in Porphyromonas gingivalis LPS-induced vascular cell adhesion molecule-1 expression in human aortic endothelial cells.

An increasing number of studies have shown a correlation between Porphyromonas gingivalis (P. gingivalis) infection and atherosclerosis. A recent study demonstrated that the expression of vascular cell adhesion molecule-1 (VCAM-1) was induced by P. gingivalis lipopolysaccharide (LPS) in human aortic endothelial cells (HAECs). The activation of p38 mitogen-activated protein kinase (p38 MAPK) was at least partially involved in this process. Those results suggested the potential involvement of P. gingivalis LPS in the pathogenesis of atherosclerosis. However, the mechanism involved in P. gingivalis LPS-induced VCAM-1 production has not yet been elucidated. The present study examined the role of the c-Jun N-terminal kinase (JNK) and nuclear factor‑κB (NF‑κB) cell signaling pathways in P. gingivalis LPS-induced VCAM-1 expression in HAECs. Western blotting was used to investigate the activation of JNK and NF‑κB pathways in HAECs exposed to P. gingivalis LPS. Following this, specific pharmacological inhibitors were introduced and the protein production of VCAM-1 was studied. The results showed that the JNK and NF‑κB pathways in HAECs were capable of being activated by P. gingivalis LPS. The inhibition of NF-κB by SN50 significantly attenuated P. gingivalis LPS-induced VCAM-1 expression, while the inhibition of JNK by SP600125 enhanced VCAM-1 expression in P. gingivalis LPS-treated HAECs. Therefore, the results indicated that NF‑κB was essential for the P. gingivalis LPS-induced VCAM-1 expression in HAECs and that JNK may be a suppressor of VCAM-1 expression in HAECs.