CITED2 Attenuates Ischemia Reperfusion-Induced Pyroptosis and Injury in Cardiomyocyte.

IF 1.2 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS International heart journal Pub Date : 2024-11-30 Epub Date: 2024-11-14 DOI:10.1536/ihj.24-060
Long Qian, Juan Zhao, Mengtao Fan, Jie Wang, Zhuqing Ji
{"title":"CITED2 Attenuates Ischemia Reperfusion-Induced Pyroptosis and Injury in Cardiomyocyte.","authors":"Long Qian, Juan Zhao, Mengtao Fan, Jie Wang, Zhuqing Ji","doi":"10.1536/ihj.24-060","DOIUrl":null,"url":null,"abstract":"<p><p>To examine the role of CITED2 in myocardial ischemia/reperfusion injury (MIRI) in a cell model and uncover the mechanism, hypoxia/reoxygenation (H/R) -stimulated H9C2 cell model was utilized as a MIRI cell model. Quantitative polymerase chain reaction (qPCR) as well as immunoblot assays were carried out to determine the expression of CITED2 in the MIRI cell model. MTT as well as lactate dehydrogenase assays were employed to detect the survival of H/R-stimulated H9C2 cells. Immunoblot, flow cytometry, qPCR, and enzyme-linked immunosorbent assay were carried out to assess the pyroptosis and inflammation in H9C2 cells. Immunoblot assays were used to confirm the mechanism. The expression of CITED2 was low in H/R-stimulated H9C2 cells. CITED2 can increase the survival of H/R-stimulated H9C2 cells. Additionally, CITED2 restrained H/R-stimulated pyroptosis of H9C2 cells. It also restrained the release of H/R-induced inflammatory factors. Mechanically, CITED2 inhibited HIF-1α expression, thereby suppressing MIRI progression. CITED2 attenuates MIRI in cardiomyocytes via mediating HIF-1α expression.</p>","PeriodicalId":13711,"journal":{"name":"International heart journal","volume":" ","pages":"1087-1094"},"PeriodicalIF":1.2000,"publicationDate":"2024-11-30","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.24-060","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/11/14 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

Abstract

To examine the role of CITED2 in myocardial ischemia/reperfusion injury (MIRI) in a cell model and uncover the mechanism, hypoxia/reoxygenation (H/R) -stimulated H9C2 cell model was utilized as a MIRI cell model. Quantitative polymerase chain reaction (qPCR) as well as immunoblot assays were carried out to determine the expression of CITED2 in the MIRI cell model. MTT as well as lactate dehydrogenase assays were employed to detect the survival of H/R-stimulated H9C2 cells. Immunoblot, flow cytometry, qPCR, and enzyme-linked immunosorbent assay were carried out to assess the pyroptosis and inflammation in H9C2 cells. Immunoblot assays were used to confirm the mechanism. The expression of CITED2 was low in H/R-stimulated H9C2 cells. CITED2 can increase the survival of H/R-stimulated H9C2 cells. Additionally, CITED2 restrained H/R-stimulated pyroptosis of H9C2 cells. It also restrained the release of H/R-induced inflammatory factors. Mechanically, CITED2 inhibited HIF-1α expression, thereby suppressing MIRI progression. CITED2 attenuates MIRI in cardiomyocytes via mediating HIF-1α expression.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
CITED2 可减轻缺血再灌注诱导的心肌细胞脓毒症和损伤。
为了在细胞模型中研究 CITED2 在心肌缺血再灌注损伤(MIRI)中的作用并揭示其机制,研究人员利用缺氧/再氧合(H/R)刺激的 H9C2 细胞模型作为 MIRI 细胞模型。研究人员通过定量聚合酶链反应(qPCR)和免疫印迹检测来确定 CITED2 在 MIRI 细胞模型中的表达。采用 MTT 和乳酸脱氢酶检测 H/R 刺激的 H9C2 细胞的存活率。免疫印迹、流式细胞术、qPCR和酶联免疫吸附试验被用来评估H9C2细胞的热休克和炎症。免疫印迹分析用于确认其机制。CITED2在H/R刺激的H9C2细胞中表达量较低。CITED2 可提高 H/R 刺激的 H9C2 细胞的存活率。此外,CITED2 还能抑制 H/R 刺激下 H9C2 细胞的热凋亡。它还能抑制 H/R 诱导的炎症因子的释放。从机制上讲,CITED2抑制了HIF-1α的表达,从而抑制了MIRI的进展。CITED2通过介导HIF-1α的表达来减轻心肌细胞的MIRI。
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 去求助
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.
期刊最新文献
Human Umbilical Cord Mesenchymal Stem Cell-Derived Exosomes Modulate the NLRP3 Inflammasome/Caspase-1 Pathway to Repress Pyroptosis Induced by Hypoxia/Reoxygenation in Cardiac Microvascular Endothelial Cells. Lifestyle Habits of Patients with Acute Myocardial Infarction and Specificity by Age Group. CITED2 Attenuates Ischemia Reperfusion-Induced Pyroptosis and Injury in Cardiomyocyte. Clinical Features and Postoperative Mobilization following Total Aortic Arch Replacement. Deep Learning to Detect Pulmonary Hypertension from the Chest X-Ray Images of Patients with Systemic Sclerosis.
×
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
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 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 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1