miR-125b-5p alleviates the damage of myocardial infarction by inhibiting the NFAT2 to reduce F2RL2 expression.

IF 2.4 4区 医学 Q4 CELL & TISSUE ENGINEERING Regenerative medicine Pub Date : 2023-07-01 DOI:10.2217/rme-2022-0150
Zhenhua Wu, Jie Geng, Yunpeng Bai, Yujuan Qi, Chao Chang, Yan Jiao, Zhigang Guo
{"title":"miR-125b-5p alleviates the damage of myocardial infarction by inhibiting the <i>NFAT2</i> to reduce <i>F2RL2</i> expression.","authors":"Zhenhua Wu,&nbsp;Jie Geng,&nbsp;Yunpeng Bai,&nbsp;Yujuan Qi,&nbsp;Chao Chang,&nbsp;Yan Jiao,&nbsp;Zhigang Guo","doi":"10.2217/rme-2022-0150","DOIUrl":null,"url":null,"abstract":"<p><p><b>Aim:</b> To explore the effect of miR-125b-5p/nuclear factor of activated T cells 1 (<i>NFAT2</i>)/<i>F2RL2</i> on myocardial infarction (MI). <b>Method:</b> After establishment of MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, the effects of <i>NFAT2</i> on the process of MI were observed, the effects of miR-125b-5p/<i>NFAT2</i>/<i>F2RL2</i> on the cell viability, apoptosis, and inflammatory factors levels were determined. <b>Result:</b> <i>NFAT2</i> silencing relieved MI and inhibited the inflammation in MI model mice. In OGD-induced human coronary artery endothelial cells and human cardiac microvascular endothelial cells, miR-125b-5p enhanced cell viability, yet repressed cell apoptosis and inflammatory factors and NFAT2 levels. NFAT2 overexpression reversed the effects of miR-125b-5p, while <i>F2RL2</i> silencing offset the effects of NFAT2 overexpression. <b>Conclusion:</b> MiR-125b-5p alleviates MI injury by inhibiting <i>NFAT2</i> level to reduce <i>F2RL2</i> expression.</p>","PeriodicalId":21043,"journal":{"name":"Regenerative medicine","volume":"18 7","pages":"543-559"},"PeriodicalIF":2.4000,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Regenerative medicine","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.2217/rme-2022-0150","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"CELL & TISSUE ENGINEERING","Score":null,"Total":0}
引用次数: 0

Abstract

Aim: To explore the effect of miR-125b-5p/nuclear factor of activated T cells 1 (NFAT2)/F2RL2 on myocardial infarction (MI). Method: After establishment of MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, the effects of NFAT2 on the process of MI were observed, the effects of miR-125b-5p/NFAT2/F2RL2 on the cell viability, apoptosis, and inflammatory factors levels were determined. Result: NFAT2 silencing relieved MI and inhibited the inflammation in MI model mice. In OGD-induced human coronary artery endothelial cells and human cardiac microvascular endothelial cells, miR-125b-5p enhanced cell viability, yet repressed cell apoptosis and inflammatory factors and NFAT2 levels. NFAT2 overexpression reversed the effects of miR-125b-5p, while F2RL2 silencing offset the effects of NFAT2 overexpression. Conclusion: MiR-125b-5p alleviates MI injury by inhibiting NFAT2 level to reduce F2RL2 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
miR-125b-5p通过抑制NFAT2,降低F2RL2的表达,减轻心肌梗死的损害。
目的:探讨miR-125b-5p/活化T细胞核因子1 (NFAT2)/F2RL2对心肌梗死(MI)的影响。方法:通过建立心肌梗死小鼠模型和氧糖剥夺(OGD)诱导的细胞模型,观察NFAT2对心肌梗死过程的影响,测定miR-125b-5p/NFAT2/F2RL2对细胞活力、凋亡及炎症因子水平的影响。结果:NFAT2沉默可减轻心肌梗死模型小鼠的心肌梗死,抑制心肌梗死模型小鼠的炎症反应。在ogd诱导的人冠状动脉内皮细胞和人心脏微血管内皮细胞中,miR-125b-5p增强了细胞活力,但抑制了细胞凋亡、炎症因子和NFAT2水平。NFAT2过表达逆转了miR-125b-5p的作用,而F2RL2沉默抵消了NFAT2过表达的作用。结论:MiR-125b-5p通过抑制NFAT2水平降低F2RL2表达来减轻心肌损伤。
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 去求助
来源期刊
Regenerative medicine
Regenerative medicine 医学-工程:生物医学
CiteScore
4.20
自引率
3.70%
发文量
82
审稿时长
6-12 weeks
期刊介绍: Regenerative medicine replaces or regenerates human cells, tissue or organs, to restore or establish normal function*. Since 2006, Regenerative Medicine has been at the forefront of publishing the very best papers and reviews covering the entire regenerative medicine sector. The journal focusses on the entire spectrum of approaches to regenerative medicine, including small molecule drugs, biologics, biomaterials and tissue engineering, and cell and gene therapies – it’s all about regeneration and not a specific platform technology. The journal’s scope encompasses all aspects of the sector ranging from discovery research, through to clinical development, through to commercialization. Regenerative Medicine uniquely supports this important area of biomedical science and healthcare by providing a peer-reviewed journal totally committed to publishing the very best regenerative medicine research, clinical translation and commercialization. Regenerative Medicine provides a specialist forum to address the important challenges and advances in regenerative medicine, delivering this essential information in concise, clear and attractive article formats – vital to a rapidly growing, multidisciplinary and increasingly time-constrained community. Despite substantial developments in our knowledge and understanding of regeneration, the field is still in its infancy. However, progress is accelerating. The next few decades will see the discovery and development of transformative therapies for patients, and in some cases, even cures. Regenerative Medicine will continue to provide a critical overview of these advances as they progress, undergo clinical trials, and eventually become mainstream medicine.
期刊最新文献
Allogeneic bone marrow derived clonal mesenchymal stromal cells in refractory rheumatoid arthritis: a pilot study. Challenges in the processing and preservation of adipose-derived stem cell subpopulations for clinical use. Risk-based pricing models and the role they might play in patients' access to new stem cell therapies. Extracellular vesicles as standard-of-care therapy: will fast-tracking the regulatory processes help achieve the goal? Artificial intelligence powers regenerative medicine into predictive realm.
×
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