MicroRNA-322-5p protects against myocardial infarction through targeting BTG2

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS

ACS Applied Bio Materials Pub Date : 2024-03-02 DOI:10.1016/j.amjms.2024.02.012

Yang Ruan MD , Shuai Meng MM , Ruofei Jia MM , Xiaojing Cao MD , Zening Jin MD

{"title":"MicroRNA-322-5p protects against myocardial infarction through targeting BTG2","authors":"Yang Ruan MD , Shuai Meng MM , Ruofei Jia MM , Xiaojing Cao MD , Zening Jin MD","doi":"10.1016/j.amjms.2024.02.012","DOIUrl":null,"url":null,"abstract":"<div><h3>Background</h3><p>Numerous studies have explored the therapeutic potential of microRNA (miR) in myocardial infarction (MI) treatment. This study focuses on the role of miR-322-5p in MI, particularly in its regulatory interaction with B-cell translocation gene 2 (BTG2).</p></div><div><h3>Materials and methods</h3><p>Expression levels of miR-322-5p and BTG2 were assessed in a rat MI model. Adenovirus altering miR-322-5p or BTG2 expression were administered to MI rats. Evaluation included cardiac function, inflammation, myocardial injury, pathological changes, apoptosis, and NF-κB pathway-related genes in MI rats post-targeted treatment. The miR-322-5p and BTG2 targeting relationship was investigated.</p></div><div><h3>Results</h3><p>MI rats exhibited low miR-322-5p and high BTG2 expression in the myocardial tissues. Restoration of miR-322-5p enhanced cardiac function, alleviated inflammation and myocardial injury, mitigated pathological changes and apoptosis, and deactivated the NF-κB pathway in MI rats. BTG2 expression was negatively-regulated by miR-322-5p. Overexpressed BTG2 counteracted miR-322-5p-induced cardioprotection on MI rats.</p></div><div><h3>Conclusion</h3><p>This study provides evidence that miR-322-5p protects against MI by suppressing BTG2 expression.</p></div>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0002962924011054","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}

引用次数: 0

Abstract

Background

Numerous studies have explored the therapeutic potential of microRNA (miR) in myocardial infarction (MI) treatment. This study focuses on the role of miR-322-5p in MI, particularly in its regulatory interaction with B-cell translocation gene 2 (BTG2).

Materials and methods

Expression levels of miR-322-5p and BTG2 were assessed in a rat MI model. Adenovirus altering miR-322-5p or BTG2 expression were administered to MI rats. Evaluation included cardiac function, inflammation, myocardial injury, pathological changes, apoptosis, and NF-κB pathway-related genes in MI rats post-targeted treatment. The miR-322-5p and BTG2 targeting relationship was investigated.

Results

MI rats exhibited low miR-322-5p and high BTG2 expression in the myocardial tissues. Restoration of miR-322-5p enhanced cardiac function, alleviated inflammation and myocardial injury, mitigated pathological changes and apoptosis, and deactivated the NF-κB pathway in MI rats. BTG2 expression was negatively-regulated by miR-322-5p. Overexpressed BTG2 counteracted miR-322-5p-induced cardioprotection on MI rats.

Conclusion

This study provides evidence that miR-322-5p protects against MI by suppressing BTG2 expression.

查看原文本刊更多论文

MicroRNA-322-5p 通过靶向 BTG2 保护心肌梗死。

背景：许多研究探讨了微RNA（miR）在心肌梗死（MI）治疗中的治疗潜力。本研究重点关注 miR-322-5p 在心肌梗死中的作用，尤其是它与 B 细胞易位基因 2（BTG2）之间的调控相互作用：方法：在大鼠 MI 模型中评估 miR-322-5p 和 BTG2 的表达水平。给心肌梗死大鼠注射改变 miR-322-5p 或 BTG2 表达的腺病毒。评估内容包括靶向治疗后 MI 大鼠的心功能、炎症、心肌损伤、病理变化、细胞凋亡和 NF-κB 通路相关基因。研究还探讨了 miR-322-5p 与 BTG2 靶向的关系：结果：心肌梗死大鼠心肌组织中 miR-322-5p 低表达，BTG2 高表达。恢复 miR-322-5p 能增强 MI 大鼠的心功能，缓解炎症和心肌损伤，减轻病理变化和细胞凋亡，并使 NF-κB 通路失活。BTG2 的表达受 miR-322-5p 的负调控。过表达的 BTG2 抵消了 miR-322-5p 诱导的心肌梗死大鼠的心脏保护作用：结论：本研究提供了 miR-322-5p 通过抑制 BTG2 表达来保护心肌梗死的证据。

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

ACS Applied Bio Materials Chemistry-Chemistry (all)

CiteScore

9.40

自引率

2.10%

发文量

464