Journal
MOLECULAR AND CELLULAR BIOCHEMISTRY
Volume 429, Issue 1-2, Pages 45-58Publisher
SPRINGER
DOI: 10.1007/s11010-016-2935-3
Keywords
MicroRNA-150; HUVECs; Apoptosis; ELK1; Atherosclerosis
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Funding
- Medical Scientific Research Foundation of Guangdong Province, China [A2016059]
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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.
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