LncRNA TUG1 Knockdown Reduces Cardiomyocyte Damage in Viral Myocarditis by Targeting the miR-140-3p/CXCL8 Axis.

IF 1.4 4区医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS

Anatolian Journal of Cardiology Pub Date : 2024-11-21 DOI:10.14744/AnatolJCardiol.2024.4523

Ji Shi, Qiyin Sun

{"title":"LncRNA TUG1 Knockdown Reduces Cardiomyocyte Damage in Viral Myocarditis by Targeting the miR-140-3p/CXCL8 Axis.","authors":"Ji Shi, Qiyin Sun","doi":"10.14744/AnatolJCardiol.2024.4523","DOIUrl":null,"url":null,"abstract":"Background: The purpose of this study was to probe the specific role of long noncoding RNA taurine upregulation 1 (LncRNA TUG1) in viral myocarditis (VMC).Methods: The mouse model of VMC was induced by Coxsackievirus type B3 (CVB3). LncRNA TUG1 was subsequently silenced, and micro-140-3p (miR-140-3p) was overexpressed in VMC mice. GenePharma synthesized wild-type and mutant LncRNA TUG1 or CXCL8 (C-X-C Motif Chemokine Ligand 8, Interleukin-8) fragments containing the miR-140-3p binding site and cloned them into the pmirGLO luciferase reporter vector. Dual luciferase reporter assays were performed to test the activity of LncRNA TUG1 or CXCL8 fragments containing miR-140-3p mimic and mimic NC. The effects of silencing LncRNA TUG1 on cell proliferation, apoptosis, and inflammation in the VMC mouse model and in vitro were investigated by flow cytometry, enzyme linked immunosorbent assay, and western blot.Results: In the VMC mouse model, LncRNA TUG1 and CXCL8 were upregulated, while miR-140-3p was downregulated. Suppressing LncRNA TUG1 led to inhibition of CXCL8 by promoting miR-140-3p. Suppressing LncRNA TUG1 or CXCL8 or restoring miR-140-3p were observed to increase cell viability and decrease apoptosis rate of cardiomyocytes.Conclusion: LncRNA TUG1 knockdown suppresses inflammation and damage of VMC cardiomyocytes via the miR-140-3p/CXCL8 axis.","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4000,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694687/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anatolian Journal of Cardiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.14744/AnatolJCardiol.2024.4523","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}

引用次数: 0

Abstract

Background: The purpose of this study was to probe the specific role of long noncoding RNA taurine upregulation 1 (LncRNA TUG1) in viral myocarditis (VMC).

Methods: The mouse model of VMC was induced by Coxsackievirus type B3 (CVB3). LncRNA TUG1 was subsequently silenced, and micro-140-3p (miR-140-3p) was overexpressed in VMC mice. GenePharma synthesized wild-type and mutant LncRNA TUG1 or CXCL8 (C-X-C Motif Chemokine Ligand 8, Interleukin-8) fragments containing the miR-140-3p binding site and cloned them into the pmirGLO luciferase reporter vector. Dual luciferase reporter assays were performed to test the activity of LncRNA TUG1 or CXCL8 fragments containing miR-140-3p mimic and mimic NC. The effects of silencing LncRNA TUG1 on cell proliferation, apoptosis, and inflammation in the VMC mouse model and in vitro were investigated by flow cytometry, enzyme linked immunosorbent assay, and western blot.

Results: In the VMC mouse model, LncRNA TUG1 and CXCL8 were upregulated, while miR-140-3p was downregulated. Suppressing LncRNA TUG1 led to inhibition of CXCL8 by promoting miR-140-3p. Suppressing LncRNA TUG1 or CXCL8 or restoring miR-140-3p were observed to increase cell viability and decrease apoptosis rate of cardiomyocytes.

Conclusion: LncRNA TUG1 knockdown suppresses inflammation and damage of VMC cardiomyocytes via the miR-140-3p/CXCL8 axis.

查看原文本刊更多论文

LncRNA TUG1敲除通过靶向 miR-140-3p/CXCL8 轴减轻病毒性心肌炎的心肌细胞损伤

背景：本研究的目的是探究长非编码RNA牛磺酸上调1（LncRNA TUG1）在病毒性心肌炎（VMC）中的特殊作用：方法：用柯萨奇病毒B3型（CVB3）诱导小鼠建立VMC模型。LncRNA TUG1随后被沉默，micro-140-3p（miR-140-3p）在VMC小鼠中过表达。GenePharma 合成了含有 miR-140-3p 结合位点的野生型和突变型 LncRNA TUG1 或 CXCL8（C-X-C Motif Chemokine Ligand 8，白细胞介素-8）片段，并将其克隆到 pmirGLO 荧光素酶报告载体中。进行了双重荧光素酶报告实验，以检测 LncRNA TUG1 或含有 miR-140-3p mimic 和 mimic NC 的 CXCL8 片段的活性。通过流式细胞术、酶联免疫吸附试验和 Western 印迹法研究了在 VMC 小鼠模型和体外沉默 LncRNA TUG1 对细胞增殖、凋亡和炎症的影响：结果：在 VMC 小鼠模型中，LncRNA TUG1 和 CXCL8 上调，而 miR-140-3p 下调。抑制 LncRNA TUG1 可通过促进 miR-140-3p 抑制 CXCL8。据观察，抑制 LncRNA TUG1 或 CXCL8 或恢复 miR-140-3p 可提高心肌细胞的存活率并降低其凋亡率：结论：敲除 LncRNA TUG1 可通过 miR-140-3p/CXCL8 轴抑制 VMC 心肌细胞的炎症和损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Anatolian Journal of Cardiology CARDIAC & CARDIOVASCULAR SYSTEMS-

CiteScore

2.30

自引率

7.70%

发文量

270

审稿时长

12 weeks

期刊介绍： The Anatolian Journal of Cardiology is an international monthly periodical on cardiology published on independent, unbiased, double-blinded and peer-review principles. The journal’s publication language is English. The Anatolian Journal of Cardiology aims to publish qualified and original clinical, experimental and basic research on cardiology at the international level. The journal’s scope also covers editorial comments, reviews of innovations in medical education and practice, case reports, original images, scientific letters, educational articles, letters to the editor, articles on publication ethics, diagnostic puzzles, and issues in social cardiology. The target readership includes academic members, specialists, residents, and general practitioners working in the fields of adult cardiology, pediatric cardiology, cardiovascular surgery and internal medicine.