MicroRNA-150 targets ELK1 and modulates the apoptosis induced by ox-LDL in endothelial cells

被引:34
作者
Qin, Bing [1 ]
Shu, Yaqing [1 ]
Xiao, Li [1 ]
Lu, Tingting [1 ]
Lin, Yinyao [1 ]
Yang, Huan [2 ]
Lu, Zhengqi [1 ]
机构
[1] Sun Yat Sen Univ, Affiliated Hosp 3, Dept Neurol, 600 Tianhe Rd, Guangzhou 510630, Guangdong, Peoples R China
[2] Cent South Univ, Xiangya Hosp, Dept Neurol, Changsha 410008, Hunan, Peoples R China
关键词
MicroRNA-150; HUVECs; Apoptosis; ELK1; Atherosclerosis; LIPOPROTEIN-INDUCED APOPTOSIS; SUPEROXIDE DISMUTASE-1; EXPRESSION; MIR-150; DYSFUNCTION; CANCER; BRAIN; ATHEROSCLEROSIS; DIFFERENTIATION; INFLAMMATION;
D O I
10.1007/s11010-016-2935-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Atherosclerosis, a chronic inflammatory disease, is the major cause of life-threatening complications such as myocardial infarction and stroke. Endothelial cells (ECs) apoptosis plays a vital role in the initiation and progression of atherosclerosis. Although a subset of microRNAs (miRNAs) have been identified as critical regulators of atherosclerosis, studies on their participation in endothelial apoptosis in atherosclerosis have been limited. In the current study, we show that miRNA-150 (miR-150) expression was substantially up-regulated during the oxidized low-density lipoprotein (ox-LDL)-induced apoptosis in human umbilical cord vein endothelial cells (HUVECs). Forced expression of miR-150 enhanced apoptosis in ECs, whereas inhibition of miR-150 could partly alleviate apoptotic cell death mediated by ox-LDL. Further analysis identified ELK1 as a direct target of miR-150, and ELK1 knockdown abolished the anti-apoptotic effect of miR-150 inhibitor. These findings reveal a novel role of miR-150 in endothelial apoptosis and indicate a therapeutic potential of miR-150 for endothelial dysfunction and atherosclerosis.
引用
收藏
页码:45 / 58
页数:14
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