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

作者：Lu, Ying; Zhu, Xiao; Liang, Gan-Xiong; Cui, Rong-Rong; Liu, Yuan; Wu, Shan-Shan; Liang, Qiu-Hua; Liu, Guan-Ying; Jiang, Yi; Liao, Xiao-Bo; Xie, Hui; Zhou, Hou-De; Wu, Xian-Ping; Yuan, Ling-Qing^*; Liao, Er-Yuan

来源：Amino Acids, 2012, 43(5): 2125-2136.

DOI：10.1007/s00726-012-1298-7

• Apelin
• Human umbilical vein endothelial cells
• Intercellular adhesion molecule-1
• Vascular cell adhesion molecule-1
• Monocyte chemotactic protein-1

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-kappa B) 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.

• 单位
  中山市人民医院; 中南大学