Apelin–APJ induces ICAM-1, VCAM-1 and MCP-1 expression via NF-κB/JNK signal pathway in human umbilical vein endothelial cells

• DOI: 10.1007/s00726-012-1298-7
• Publication Date: 2012-04-24T08:36:29Z
• Authors: Ying Lu; Xiao Zhu; Gan-Xiong Liang; Rong-Rong Cui; Yuan Liu; Shan-Shan Wu; Qiu-Hua Liang; Guan-Ying Liu; Yi Jiang; Xiao-Bo Liao; Hui Xie; Hou-De Zhou; Xian-Ping Wu; Ling-Qing Yuan; Er-Yuan Liao
• Keywords: VCAM-1; Apelin; Intercellular adhesion molecule

Apelin receptor (APJ) deficiency has been reported to be preventive against atherosclerosis. However, the mechanism of this effect remains unknown. In this study, quantitative real-time RT-PCR, Western blotting and ELISA analyses revealed a significant increase in the expression of intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) treated with apelin. Inhibitors of cellular signal transduction molecules were used to demonstrate involvement of nuclear factor kappa-B (NF-κB) and c-Jun N-terminal kinase (JNK) pathways in apelin-APJ-induced activation of adhesion molecules and chemokines. Inhibition of APJ expression by RNA interference abrogated apelin-induced expression of adhesion molecules and chemokines and apelin-stimulated cellular signal transduction in HUVECs. The apelin-APJ system in endothelial cells is involved in the expression of adhesion molecules and chemokines, which are important for the initiation of endothelial inflammation-related atherosclerosis. Therefore, apelin-APJ and the cell signaling pathways activated by this system in endothelial cells may represent targets for therapy of atherosclerosis.