Abstract:
:Oxidized low density lipoprotein (ox-LDL) and lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) have been implicated in the development of atherosclerosis. This study was designed to investigate the expression regulation of LOX-1 by ox-LDL and the potential underlying mechanisms in cultured rat vascular smooth muscle cells (VSMCs). VSMCs were treated with ox-LDL, and the expressions of LOX-1 mRNA and proteins were determined by RT-PCR and western blotting, respectively. The intracellular reactive oxygen species (ROS) production was monitored by flow cytometry with fluorescence probe, DCFH(2) -DA. The effect of several inhibitors including aspirin, NDGA, allopurinol, apocynin, and rotenone on ox-LDL-induced ROS formation and LOX-1 expression was also investigated. The roles of NF-κB p65 and JNK were explored. Ox-LDL significantly induced LOX-1 expression at both mRNA and protein levels in a dose-dependent and time-dependent manner. Aspirin, NDGA, and preconditioned apocynin suppressed ox-LDL-induced intracellular ROS production and LOX-1 expression, while allopurinol and rotenone failed to do so. Vitamin C and N-acetyl-l-cysteine demonstrated similar effect. Furthermore, both NF-κB p65 expression and phosphorylated JNK (p-JNK) to JNK expression ratio were elevated after ox-LDL treatment. In addition, the NF-κB inhibitor PDTC and JNK inhibitor SP600125 pretreatment partly abolished ox-LDL-induced LOX-1 expression. These findings suggested that ROS mediated ox-LDL-induced LOX-1 expression in VSMCs through NF-κB and JNK signaling pathways.
journal_name
Fundam Clin Pharmacoljournal_title
Fundamental & clinical pharmacologyauthors
Sun Y,Chen Xdoi
10.1111/j.1472-8206.2010.00885.xsubject
Has Abstractpub_date
2011-10-01 00:00:00pages
572-9issue
5eissn
0767-3981issn
1472-8206journal_volume
25pub_type
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