LncRNA MIR17HG alleviates heart failure via targeting MIR17HG/miR-153-3p/SIRT1 axis in in vitro model

IF 2.1 4区化学 Q3 CHEMISTRY, MULTIDISCIPLINARY

Open Chemistry Pub Date : 2024-07-26 DOI:10.1515/chem-2023-0146

Shuai Sun, Jianxin Weng, Yun Chen, Tingting Zheng, Yan Li, Jianfei Zhu, Yanjun Chen

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引用次数: 0

Abstract

Heart failure (HF) is a syndrome of symptoms and signs caused by cardiac insufficiency and have become a serious global health problem. The aim of this study is to clarify the role and mechanism failure of MIR17HG. We established the in vitro HF model by using H2O2-treated AC-16 and HCM cells, and the reactive oxygen species (ROS) level and natriuretic peptide precursor B (NPPB) expression were also detected. The RNA expression of MIR17HG, miR-153-3p, SIRT1, and NPPB were detected by quantitative reverse transcription PCR while the SIRT1 and NPPB expression were detected by western blot. The binding relationship among MIR17HG, miR-153-3p, and SIRT1 were assessed by dual-luciferase reporter assay and RNA binding protein immunoprecipitation assay. Then, MIR17HG and SIRT1 were overexpressed by lentivirus transfection, and the influence of MIR17HG and SIRT1 on H2O2-induced apoptosis mediated by p53 were evaluated. The results show that MIR17HG and SIRT1 were significantly downregulated, while miR-153-3p was significantly upregulated in HF model. Overexpression of MIR17HG reduced miR-153-3p and alleviated HF, while knockdown of SIRT1 weakened the effects of MIR17HG, suggesting that SIRT1 was the direct target of MIR17HG/miR-153-3p axis. MIR17HG is significantly downregulated in HF model. Our research shows that MIR17HG protects cardiomyocytes from ROS-induced damage via the MIR17HG/miR-153-3p/SIRT1 axis, suggesting that MIR17HG and SIRT1 are potential therapeutic targets in HF.

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体外模型中，LncRNA MIR17HG通过靶向MIR17HG/miR-153-3p/SIRT1轴缓解心衰

心力衰竭（HF）是由心功能不全引起的症状和体征综合征，已成为一个严重的全球性健康问题。本研究旨在阐明 MIR17HG 的作用和失效机制。我们利用经 H2O2 处理的 AC-16 和 HCM 细胞建立了体外高频模型，并检测了活性氧（ROS）水平和钠尿肽前体 B（NPPB）的表达。反转录定量 PCR 检测了 MIR17HG、miR-153-3p、SIRT1 和 NPPB 的 RNA 表达，Western 印迹检测了 SIRT1 和 NPPB 的表达。通过双荧光素酶报告实验和 RNA 结合蛋白免疫沉淀实验评估了 MIR17HG、miR-153-3p 和 SIRT1 之间的结合关系。然后，通过慢病毒转染过表达MIR17HG和SIRT1，评估MIR17HG和SIRT1对p53介导的H2O2诱导细胞凋亡的影响。结果显示，在高频模型中，MIR17HG和SIRT1被显著下调，而miR-153-3p被显著上调。过表达MIR17HG可降低miR-153-3p并缓解HF，而敲除SIRT1可削弱MIR17HG的作用，这表明SIRT1是MIR17HG/miR-153-3p轴的直接靶标。MIR17HG在高频模型中明显下调。我们的研究表明，MIR17HG通过MIR17HG/miR-153-3p/SIRT1轴保护心肌细胞免受ROS诱导的损伤，这表明MIR17HG和SIRT1是HF的潜在治疗靶点。

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来源期刊

Open Chemistry CHEMISTRY, MULTIDISCIPLINARY-

CiteScore

3.80

自引率

4.30%

发文量

审稿时长

6 weeks

期刊介绍： Open Chemistry is a peer-reviewed, open access journal that publishes original research, reviews and short communications in the fields of chemistry in an ongoing way. The central goal is to provide a hub for researchers working across all subjects to present their discoveries, and to be a forum for the discussion of the important issues in the field. The journal is the premier source for cutting edge research in fundamental chemistry and it provides high quality peer review services for its authors across the world. Moreover, it allows for libraries everywhere to avoid subscribing to multiple local publications, and to receive instead all the necessary chemistry research from a single source available to the entire scientific community.