Clinical Significance and Potential Mechanism of Circ_00008842 in Acute Myocardial Infarction

IF 1.2 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS
Li Zhang, Ming Wang, Ran Liao, Qing Han
{"title":"Clinical Significance and Potential Mechanism of Circ_00008842 in Acute Myocardial Infarction","authors":"Li Zhang, Ming Wang, Ran Liao, Qing Han","doi":"10.1536/ihj.24-009","DOIUrl":null,"url":null,"abstract":"</p><p>This study aimed to evaluate the clinical value of circ_0008842 in acute myocardial infarction (AMI) and explore the potential mechanisms.</p><p>GSE149051 and GSE160717 datasets analyze common differentially expressed circRNAs (coDEcircRNA) in AMI. RT-qPCR analysis of circ_0008842 mRNA levels in patients with AMI. ROC curve assesses the diagnostic value of circ_0008842 in AMI. A cell model of AMI was constructed by hypoxia-reoxygenation (H/R) -induced H9c2. Cell viability and apoptosis were examined by CCK-8 and flow cytometry. Enzyme-linked immunosorbent assay was used to explore myocardial injury markers CK-MB and cTnI secretion. Dual luciferase reporter assays validate circ_0008842 binding to miRNA. PPI network and gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment reveal potential functions and pathways of targets from the miRNA in AMI.</p><p>circ_0008842 is recognized as coDEcircRNA in AMI-related databases. circ_0008842 was greatly lower and miR-574-5p was significantly higher in patients with AMI than in healthy individuals. miR-574-5p is a target of circ_0008842. The sensitivity and specificity of circ_0008842 for diagnosing patients with AMI were 87.40% and 83.50%, respectively. Overexpression of circ_0008842 inhibited H/R induced apoptosis, increased cell viability, and decreased CK-MB and cTnI levels, which were partially abrogated by overexpression of miR-574-5p. Calmodulin-like protein 4 (CALML4) was the most connected hub gene in the PPI network of miR-574-5p predicted target genes.</p><p>circ_0008842 is a diagnostic biomarker for AMI and participates in myocardial injury in AMI by regulating miR-574-5p. Our study provides new insights into the diagnosis for AMI.</p>\n<p></p>","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":null,"pages":null},"PeriodicalIF":1.2000,"publicationDate":"2024-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International heart journal","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1536/ihj.24-009","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

This study aimed to evaluate the clinical value of circ_0008842 in acute myocardial infarction (AMI) and explore the potential mechanisms.

GSE149051 and GSE160717 datasets analyze common differentially expressed circRNAs (coDEcircRNA) in AMI. RT-qPCR analysis of circ_0008842 mRNA levels in patients with AMI. ROC curve assesses the diagnostic value of circ_0008842 in AMI. A cell model of AMI was constructed by hypoxia-reoxygenation (H/R) -induced H9c2. Cell viability and apoptosis were examined by CCK-8 and flow cytometry. Enzyme-linked immunosorbent assay was used to explore myocardial injury markers CK-MB and cTnI secretion. Dual luciferase reporter assays validate circ_0008842 binding to miRNA. PPI network and gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment reveal potential functions and pathways of targets from the miRNA in AMI.

circ_0008842 is recognized as coDEcircRNA in AMI-related databases. circ_0008842 was greatly lower and miR-574-5p was significantly higher in patients with AMI than in healthy individuals. miR-574-5p is a target of circ_0008842. The sensitivity and specificity of circ_0008842 for diagnosing patients with AMI were 87.40% and 83.50%, respectively. Overexpression of circ_0008842 inhibited H/R induced apoptosis, increased cell viability, and decreased CK-MB and cTnI levels, which were partially abrogated by overexpression of miR-574-5p. Calmodulin-like protein 4 (CALML4) was the most connected hub gene in the PPI network of miR-574-5p predicted target genes.

circ_0008842 is a diagnostic biomarker for AMI and participates in myocardial injury in AMI by regulating miR-574-5p. Our study provides new insights into the diagnosis for AMI.

Circ_00008842 在急性心肌梗死中的临床意义和潜在机制
这项研究旨在评估circ_0008842在急性心肌梗死(AMI)中的临床价值,并探索其潜在机制。GSE149051和GSE160717数据集分析了AMI中常见的差异表达circRNA(coDEcircRNA)。对 AMI 患者中 circ_0008842 mRNA 水平的 RT-qPCR 分析。ROC 曲线评估了 circ_0008842 在 AMI 中的诊断价值。通过缺氧-复氧(H/R)诱导的 H9c2 构建了 AMI 的细胞模型。通过 CCK-8 和流式细胞术检测细胞活力和凋亡。酶联免疫吸附试验用于检测心肌损伤标志物 CK-MB 和 cTnI 的分泌。双荧光素酶报告实验验证了 circ_0008842 与 miRNA 的结合。PPI网络和基因本体论以及京都基因和基因组百科全书的通路富集揭示了miRNA在AMI中的潜在功能和靶标通路,circ_0008842在AMI相关数据库中被认定为coDEcircRNA,Circ_0008842在AMI患者中的含量大大低于健康人,而miR-574-5p则明显高于健康人。circ_0008842 对诊断 AMI 患者的敏感性和特异性分别为 87.40% 和 83.50%。过表达circ_0008842可抑制H/R诱导的细胞凋亡,提高细胞活力,降低CK-MB和cTnI水平,而过表达miR-574-5p可部分缓解这些作用。在miR-574-5p预测靶基因的PPI网络中,钙调蛋白样蛋白4(CALML4)是连接最紧密的枢纽基因。circ_0008842是AMI的诊断生物标志物,通过调控miR-574-5p参与AMI的心肌损伤。我们的研究为AMI的诊断提供了新的见解。
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
International heart journal
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
期刊介绍: Authors of research articles should disclose at the time of submission any financial arrangement they may have with a company whose product figures prominently in the submitted manuscript or with a company making a competing product. Such information will be held in confidence while the paper is under review and will not influence the editorial decision, but if the article is accepted for publication, the editors will usually discuss with the authors the manner in which such information is to be communicated to the reader.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信