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长链非编码 RNA XIST 通过靶向 miR-873-5p/MCL1 轴调节心肌细胞凋亡。

Long noncoding RNA XIST regulates cardiomyocyte apoptosis by targeting miR-873-5p/MCL1 axis.

机构信息

Department of Cardiovascular Surgery, Shanghai Changhai Hospital, The Second Military Medical University, Shanghai, China.

出版信息

Eur Rev Med Pharmacol Sci. 2020 Dec;24(24):12878-12886. doi: 10.26355/eurrev_202012_24191.

DOI:10.26355/eurrev_202012_24191
PMID:33378038
Abstract

OBJECTIVE

The purpose of this study was to investigate the expression of miR-873-5p and long non-coding RNA X-inactive specific transcript (lncRNA-XIST) in myocardial infarction (MI), the interaction mechanism and the effect of target gene MCL1 on apoptosis in H9c2 cells.

MATERIALS AND METHODS

quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was used to detect and compare the expressions of miR-873-5p and lncRNA XIST in 8 myocardial infarction rats and 8 normal rats tissues, respectively, and the correlation between the expressions of miR-873-5p and lncRNA XIST in the myocardial tissues was explored. Next, qRT-PCR and Western blot were used to detect the effects of upregulation of miR-873-5p and downregulation of lncRNA XIST, as well as the impacts of their interactions on the expression level of MCL1 in H9c2 cells and the apoptosis of cells.

RESULTS

It was found that the downregulation of miR-873-5p protected the heart against apoptosis after AMI, and lncRNA XIST inhibited apoptosis in H9c2 cells after hypoxia. Besides, inhibiting lncRNA XIST could upregulate miR-873-5p and downregulate MCL1, thus increasing apoptosis in the H9c2 cells after hypoxia.

CONCLUSIONS

LncRNA XIST can regulate cardiomyocyte apoptosis by targeting miR-873-5p.

摘要

目的

本研究旨在探讨微小 RNA-873-5p(miR-873-5p)和长链非编码 RNA X 失活特异性转录本(lncRNA-XIST)在心肌梗死(MI)中的表达、相互作用机制以及靶基因 MCL1 对 H9c2 细胞凋亡的影响。

材料与方法

采用实时定量聚合酶链反应(qRT-PCR)检测和比较 8 只心肌梗死大鼠和 8 只正常大鼠组织中 miR-873-5p 和 lncRNA XIST 的表达,并探讨心肌组织中 miR-873-5p 和 lncRNA XIST 表达的相关性。接下来,采用 qRT-PCR 和 Western blot 检测 miR-873-5p 上调和 lncRNA XIST 下调及其相互作用对 H9c2 细胞中 MCL1 表达水平和细胞凋亡的影响。

结果

研究发现,miR-873-5p 下调可保护 AMI 后心脏免受细胞凋亡,lncRNA XIST 可抑制缺氧状态下 H9c2 细胞的凋亡。此外,抑制 lncRNA XIST 可上调 miR-873-5p 并下调 MCL1,从而增加缺氧状态下 H9c2 细胞的凋亡。

结论

lncRNA XIST 可通过靶向 miR-873-5p 调节心肌细胞凋亡。

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