title: Apelin-APJ induces ICAM-1, VCAM-1 and MCP-1 expression via NF-κB/JNK signal pathway in human umbilical vein endothelial cells.
abstract: 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.
authors.affiliation: Department of Endocrinology, People's Hospital of Zhongshan City, Zhongshan, Guangdong, 528403, People's Republic of China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Lu
authors.forename: Xiao
authors.initials: X
authors.lastname: Zhu
authors.forename: Gan-Xiong
authors.initials: GX
authors.lastname: Liang
authors.forename: Rong-Rong
authors.initials: RR
authors.lastname: Cui
authors.forename: Yuan
authors.initials: Y
authors.lastname: Liu
authors.forename: Shan-Shan
authors.initials: SS
authors.lastname: Wu
authors.forename: Qiu-Hua
authors.initials: QH
authors.lastname: Liang
authors.forename: Guan-Ying
authors.initials: GY
authors.lastname: Liu
authors.forename: Yi
authors.initials: Y
authors.lastname: Jiang
authors.forename: Xiao-Bo
authors.initials: XB
authors.lastname: Liao
authors.forename: Hui
authors.initials: H
authors.lastname: Xie
authors.forename: Hou-De
authors.initials: HD
authors.lastname: Zhou
authors.forename: Xian-Ping
authors.initials: XP
authors.lastname: Wu
authors.forename: Ling-Qing
authors.initials: LQ
authors.lastname: Yuan
authors.forename: Er-Yuan
authors.initials: EY
authors.lastname: Liao
mesh_terms: D000073861:Apelin; D000075244:Apelin Receptors; D015153:Blotting, Western; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000235:genetics* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005786:Gene Expression Regulation / Q000187:drug effects; D061307:Human Umbilical Vein Endothelial Cells / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins / Q000494:pharmacology*; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D043562:Receptors, G-Protein-Coupled / Q000037:antagonists & inhibitors / Q000235:genetics* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D019010:Vascular Cell Adhesion Molecule-1 / Q000235:genetics* / Q000378:metabolism
chemical_list: C115436:APLN protein, human; C104575:APLNR protein, human; D000073861:Apelin; D000075244:Apelin Receptors; C111835:CCL2 protein, human; D018932:Chemokine CCL2; D036341:Intercellular Signaling Peptides and Proteins; D016328:NF-kappa B; D034741:RNA, Small Interfering; D043562:Receptors, G-Protein-Coupled; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D048031:JNK Mitogen-Activated Protein Kinases