Journal
AMINO ACIDS
Volume 43, Issue 5, Pages 2125-2136Publisher
SPRINGER WIEN
DOI: 10.1007/s00726-012-1298-7
Keywords
Apelin; Human umbilical vein endothelial cells; Intercellular adhesion molecule-1; Vascular cell adhesion molecule-1; Monocyte chemotactic protein-1
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Funding
- National Natural Science Foundation of China [30801174, 81070246, 30900622]
- China Postdoctoral Science Foundation [20100471240]
- Ph.D. Programs Foundation of Ministry of Education of China [200805331017]
- Clinic Medicine Special Research Fund-Endocrinology Disease Research Fund of Chinese Medical Association [10020040226]
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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.
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