Long noncoding RNA NEAT1 sponges miR-125a-5p to suppress cardiomyocyte apoptosis via BCL2L12

被引:30
|
作者
Yan, Hong [1 ]
Liang, Huasheng [1 ]
Liu, Lie [1 ]
Chen, Dongli [1 ]
Zhang, Qianhuan [1 ]
机构
[1] Guangdong Gen Hosp, Guangdong Acad Med Sci, Guangdong Cardiovasc Res Inst, Dept Cardiol, 96 Dongchuan Rd, Guangzhou 510515, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
cardiomyocyte apoptosis; long non-coding RNA nuclear paraspeckle assembly transcript 1; microRNA-125a-5p; B-cell lymphoma-2-like 12; PROLIFERATION; INHIBITION; DISEASE; CANCER; INJURY;
D O I
10.3892/mmr.2019.10095
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Increasing evidence has suggested that long non-coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. The present study indicated that NEAT1 expression is markedly downregulated in cardiomyocytes following ischemia/reperfusion injury in vivo and hydrogen peroxide treatment in vitro. Further experiments suggested that ectopic overexpression of NEAT1 suppresses cardiomyocyte apoptosis induced by hydrogen peroxide, as assessed by TUNEL assay and flow cytometry. In addition, using a dual-luciferase reporter assay, NEAT1 was demonstrated to directly interact with microRNA (miR)-125a-5p and overexpression of miR-125a-5p efficiently reversed the stimulatory effect of NEAT1 on B-cell lymphoma-2-like 12 (BCL2L12) expression. Furthermore, the results indicated that NEAT1 inhibits cardiomyocyte apoptosis via regulating the expression of BCL2L12, which appeared to be mediated via miR-125a-5p. In conclusion, the present study suggested that NEAT1 functions as a miR sponge to inhibit cardiomyocyte apoptosis and may be a novel therapeutic target for cardiomyocyte apoptosis-associated heart diseases.
引用
收藏
页码:4468 / 4474
页数:7
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