LncRNA MEG3-derived miR-361-5p regulate vascular smooth muscle cells proliferation and apoptosis by targeting ABCA1

被引:8
|
作者
Wang, Minghui [1 ]
Li, Chao [2 ]
Zhang, Ying [1 ]
Zhou, Xiujun [1 ]
Liu, Yujie [1 ]
Lu, Chengzhi [2 ]
机构
[1] Tianjin Chest Hosp, Dept Cardiol, 261 Taierzhuang South Rd, Tianjin 300222, Peoples R China
[2] Tianjin First Ctr Hosp, Dept Cardiol, 26 Fukang Rd, Tianjin 300192, Peoples R China
来源
关键词
LncRNA MEG3; proliferation; apoptosis; ABCA1; vascular smooth muscle cells; LONG NONCODING RNA; MIGRATION; MEG3; ATHEROSCLEROSIS; CARCINOMA; ACTIVATION; FEATURES; MIRNAS; INJURY; VSMCS;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background: Atherosclerosis remains a leading cause of cardiology disease worldwide, which vascular smooth muscle cells (VSMCs) proliferation and apoptosis are involved. Increasing evidences have revealed that long non-coding RNAs (lncRNAs) considered to be critical regulatory factors of VSMCs function. However, the molecular mechanism is not fully understood. Methods: First, we establish the ox-LDL induced VSMC model. We conducted RT-PCR to measure MEG3 expression and miR-361-5p expression in this model. The proliferation and apoptosis of VSMCs were measured via CCK-8 proliferative assay and flow cytometry respectively. We used knockdown and overexpression system to identify the molecular mechanism. In addition, luciferase report assay and bioinformatics analysis were used to confirm the bio-target of different factors. Results: LncRNA MEG3 was down-regulated and related with miR-361-5p expression in ox-LDL injured VSMCs. Inhibition of lncRNA MEG3 promotes the proliferation and decelerates apoptosis of VSMCs. Moreover, MEG3 acts as a competing endogenous RNA (ceRNA) for miR-361-5p and further regulate ABCA1 expression regulate proliferation and apoptosis in ox-LDL injured VSMCs. Conclusion: These results suggest that LncRNA MEG3 regulate proliferation and apoptosis in ox-LDL injured VSMCs and function as a ceRNA for miR-361-5p to modulate ABCA1 expression.
引用
收藏
页码:3600 / 3609
页数:10
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