American Journal of Translational Research | |
Long noncoding RNA OIP5-AS1 accelerates the ox-LDL mediated vascular endothelial cells apoptosis through targeting GSK-3β via recruiting EZH2 | |
Yujie Liu1  Chao Li2  Minghui Wang3  | |
[1] Department of Cardiology, Tianjin Chest Hospital, Tianjin 300222, China;Department of Cardiology, Tianjin First Center Hospital, Tianjin 300192, China;Tianjin Medical University, Tianjin 300070, China | |
关键词: Vascular endothelial cells; OIP5-AS1; EZH2; ox-LDL; GSK-3β; | |
DOI : | |
学科分类:医学(综合) | |
来源: e-Century Publishing Corporation | |
【 摘 要 】
An increasing amount of research is demonstrating the role of long noncoding RNAs (lncRNAs) in human cardiovascular disease, and in particular, atherosclerosis. To date, the mechanism through which lncRNA OIP5-AS1 regulates the oxidative low-density lipoprotein (ox-LDL)-mediated endothelial cell apoptosis is still unclear. Results from this study found that lncRNA OIP5-AS1 was significantly over-expressed in the human umbilical vein endothelial cells (HUVECs) administered with ox-LDL. The silencing of OIP5-AS1 inhibited apoptosis and promoted proliferation via inducing G0/G1 cycle arrest. Chromatin immunoprecipitate (ChIP) revealed that lncRNA OIP5-AS1 reduced GSK-3β expression through recruiting EZH2, a critical element of the Polycomb Repressive Complex 2 (PRC2) complex that directly bind with the GSK-3β promoter region. Rescue experiments validated that GSK-3β could eliminate the effect of OIP5-AS1 on HUVECs. Overall, these findings suggest that lncRNA OIP5-AS1 accelerates ox-LDL mediated vascular endothelial cell apoptosis through targeting GSK-3β via recruiting EZH2, providing potential therapeutic strategies for atherosclerosis.
【 授权许可】
CC BY-NC
【 预 览 】
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