LncRNA Peg13 Alleviates Myocardial Infarction/Reperfusion Injury through Regulating MiR-34a/Sirt1-Mediated Endoplasmic Reticulum Stress

IF 1.2 4区医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS

International heart journal Pub Date : 2024-05-31 DOI:10.1536/ihj.23-453

Yonghong Wang, Jian Luo, Huiqiong Yang, Yanfei Liu

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引用次数: 0

Abstract

Myocardial infarction/reperfusion (I/R) injury significantly impacts the health of older individuals. We confirmed that the level of lncRNA Peg13 was downregulated in I/R injury. However, the detailed function of Peg13 in myocardial I/R injury has not yet been explored.

To detect the function of Peg13, in vivo model of I/R injury was constructed. RT-qPCR was employed to investigate RNA levels, and Western blotting was performed to assess levels of endoplasmic reticulum stress and apoptosis-associated proteins. EdU staining was confirmed to assess the cell proliferation.

I/R therapy dramatically produced myocardial injury, increased the infarct area, and decreased the amount of Peg13 in myocardial tissues of mice. In addition, hypoxia/reoxygenation (H/R) notably induced the apoptosis and promoted the endoplasmic reticulum (ER) stress of HL-1 cells, while overexpression of Peg13 reversed these phenomena. Additionally, Peg13 may increase the level of Sirt1 through binding to miR-34a. Upregulation of Peg13 reversed H/R-induced ER stress via regulation of miR-34a/Sirt1 axis.

LncRNA Peg13 reduces ER stress in myocardial infarction/reperfusion injury through mediation of miR-34a/Sirt1 axis. Hence, our research might shed new lights on developing new strategies for the treatment of myocardial I/R injury.

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LncRNA Peg13 通过调节 MiR-34a/Sirt1 介导的内质网应激减轻心肌梗死/再灌注损伤

心肌梗死/再灌注（I/R）损伤严重影响老年人的健康。我们证实，lncRNA Peg13的水平在I/R损伤中下调。为了检测Peg13的功能，我们构建了I/R损伤的体内模型。为了检测Peg13的功能，研究人员构建了I/R损伤体内模型，采用RT-qPCR检测RNA水平，并进行Western印迹以评估内质网应激和细胞凋亡相关蛋白的水平。I/R疗法会显著造成心肌损伤，增加梗死面积，减少小鼠心肌组织中Peg13的含量。此外，缺氧/复氧（H/R）显著诱导 HL-1 细胞凋亡并促进内质网（ER）应激，而过表达 Peg13 则可逆转这些现象。此外，Peg13 还可能通过与 miR-34a 结合提高 Sirt1 的水平。LncRNA Peg13通过调控miR-34a/Sirt1轴降低心肌梗死/再灌注损伤中的ER应激。因此，我们的研究可能为开发治疗心肌I/R损伤的新策略提供新的启示。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International heart journal 医学-心血管系统

CiteScore

2.50

自引率

6.70%

发文量

148

审稿时长

6-12 weeks

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