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首页> 外文期刊>RSC Advances >Knockdown of TUG1 aggravates hypoxia-induced myocardial cell injury via regulation of miR-144-3p/Notch1
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Knockdown of TUG1 aggravates hypoxia-induced myocardial cell injury via regulation of miR-144-3p/Notch1

机译：Tug1的敲低通过MIR-144-3P / NOTCH1加剧缺氧诱导的心肌细胞损伤

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摘要

Myocardial infarction is a common cause of mortality in cardiovascular diseases. Long noncoding RNA taurine-upregulated gene 1 (TUG1) has been reported to play an important role in the regulation of myocardial injury; however, the mechanism via which TUG1 participates in myocardial infarction is unknown. In this study, hypoxia-treated cardiomyoblast H9c2 cells were used as a model of myocardial infarction. Cell transfection was conducted using Lipofectamine 2000 for 48 h. Hypoxia-induced injury was investigated by cell viability and apoptosis using the trypan blue exclusion method, flow cytometry and Western blot. The expressions of TUG1, microRNA-144-3p (miR-144-3p) and the Notch1 pathway were investigated by a quantitative real-time polymerase chain reaction and Western blot. The association between miR-144-3p and TUG1 or Notch1 was analyzed by bioinformatics analysis and luciferase reporter assay. Our results showed that hypoxia-induced H9c2 cell injury led to the inhibition of cell viability and promotion of apoptosis. Moreover, hypoxia could cause the up-regulation of TUG1 and Notch1 expression and down-regulation of miR-144-3p. The knockdown of TUG1 or overexpression of miR-144-3p aggravated the hypoxia-induced viability suppression and apoptosis production in the H9c2 cells. Moreover, miR-144-3p was indicated to be bound to TUG1, and its abrogation reversed the silencing of TUG1-mediated promotion of hypoxia-induced injury. In addition, Notch1 was a target of miR-144-3p, and its restoration attenuated the miR-144-3p-mediated promotion of hypoxia-induced injury. Moreover, TUG1 interference alleviated the hypoxia-induced activation of the Notch1/Hes-1 pathway via the regulation of miR-144-3p. In conclusion, the interference of TUG1 contributed to hypoxia-induced injury via the regulation of the miR-144-3p/Notch1/Hes-1 pathway; this indicated a novel mechanism for understanding the pathogenesis of myocardial infarction.
机译：心肌梗塞是心血管疾病中死亡率的常见原因。据报道，长的非致RNA牛磺酸上调的基因1（Tug1）在心肌损伤的调节中发挥着重要作用;然而，Tug1参与心肌梗死的机制是未知的。在该研究中，使用缺氧治疗的心肌细胞H9C2细胞作为心肌梗死的模型。使用Lipofectamine 2000进行48小时进行细胞转染。使用台盼蓝排除方法，流式细胞术和Western印迹，通过细胞活力和细胞凋亡来研究缺氧诱导的损伤。通过定量的实时聚合酶链反应和Western印迹研究了Tug1，MicroRNA-144-3P（miR-144-3p）和Notch1途径的表达。通过生物信息学分析和荧光素酶报告器测定分析miR-144-3P和Tug1或Notch1之间的关联。我们的研究结果表明，缺氧诱导的H9C2细胞损伤导致抑制细胞活力和促进细胞凋亡。此外，缺氧可能导致Tug1和Notch1表达和下调miR-144-3p的上调和下调。 MiR-144-3P的Tug1或过表达的敲低加剧了H9C2细胞中缺氧诱导的活力抑制和凋亡产生。此外，MIR-144-3P被指示与TuG1结合，其废除逆转Tug1介导的缺氧诱导损伤的沉默。此外，Notch1是miR-144-3p的靶标，其恢复减弱了MiR-144-3P介导的缺氧诱导损伤的促进。此外，Tug1干扰通过MiR-144-3P的调节减轻了缺氧诱导的Notch1 / HER-1途径的活化。总之，Tug1的干扰通过MIR-144-3P / NOTCH1 / HER-1途径的调节导致缺氧诱导的损伤;这表明了理解心肌梗死发病机制的新机制。

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  • 来源
    《RSC Advances》 |2019年第40期|共11页
  • 作者

    Zhu Bo; Xia Zhen; Xia Zirong; Li Qing; Han Lu; Li Fan; Dong Quanbin; Li Juxiang;

  • 作者单位

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

    Nanchang Univ Affiliated Hosp 2 Dept Cardiol 1 Minde Rd Nanchang Jiangxi Peoples R China;

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  • 正文语种 eng
  • 中图分类 化学;
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