Role of p38 Mitogen‐Activated Protein Kinase Pathway in <i>Porphyromonas gingivalis</i> Lipopolysaccharide–Induced VCAM‐1 Expression in Human Aortic Endothelial Cells

Abstract

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.