Role of p38 mitogen-activated protein kinase pathway in Porphyromonas gingivalis lipopolysaccharide-induced VCAM-1 expression in human aortic endothelial cells

Background: Porphyromonas gingivalis (Pg) lipopolysaccharide (LPS) has been reported to induce the expression of vascular cell adhesion molecule‐1 (VCAM‐1) in vascular endothelial cells. This finding suggests the potential roles for Pg in the pathogenesis of atherosclerosis. However, the mechanism involved in Pg LPS‐induced VCAM‐1 production in endothelial cells remains unclear. Methods: Quantitative real‐time polymerase chain reaction and Western blotting were used, respectively, to investigate the mRNA expression and protein production of VCAM‐1 in human aortic endothelial cells (HAECs) induced by Pg LPS. The involvement of the p38 mitogen‐activated protein kinase (p38 MAPK) cell signaling pathway in VCAM‐1 expression was investigated by assays with specific inhibitors. Results: Pg LPS–induced expression in HAECs of VCAM‐1 occurred in a dose‐ and time‐dependent manner. In addition, the p38 MAPK inhibitor (SB 203580) significantly attenuated Pg LPS–induced VCAM‐1 expression. Conclusion: Activation of p38 MAPK is at least partially involved in Pg LPS–induced VCAM‐1 expression in HAECs, which may contribute to the acceleration of atherosclerosis.