LncRNA Myocardial Infarction-Associated Transcript (MIAT)/miR-505-5p Axis Regulates Proliferation and Migration of Vascular Smooth Muscle Cells of Hypertension Mice

IF 4.7 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-05-01 DOI:10.1166/jbn.2024.3824
Hua Yang, Hongfei Song, Pan Xiong
{"title":"LncRNA Myocardial Infarction-Associated Transcript (MIAT)/miR-505-5p Axis Regulates Proliferation and Migration of Vascular Smooth Muscle Cells of Hypertension Mice","authors":"Hua Yang, Hongfei Song, Pan Xiong","doi":"10.1166/jbn.2024.3824","DOIUrl":null,"url":null,"abstract":"To clarify the role of long non-coding RNA (lncRNA) MIAT in regulating proliferative and migratory abilities in VSMCs extracted from hypertension mice via downregulating microRNA-505-5p (miR-505-5p). Serum levels of MIAT and miR-505-5p in enrolled 20 hypertension patients and 20 healthy\n volunteers were detected. VSMCs were extracted from hypertension mice and healthy mice. Regulatory effects of MIAT and miR-505-5p on proliferative and migratory abilities in VSMCs were examined. At last, the interaction between MIAT and miR-505-5p was explored by dual-luciferase reporter assay\n and rescue experiments. Serum level of MIAT was higher in hypertension patients than those of healthy subjects, while miR-505-5p was downregulated. MIAT level was negatively correlated to miR-505-5p level in serum of hypertension patients. Knockdown of MIAT suppressed proliferative and migratory\n abilities in VSMCs extracted from hypertension mice. In addition, knockdown of MIAT upregulated E-cadherin and downregulated Vimentin and Snail-1. MiR-505-5p was verified to be the target binding MIAT. Knockdown of miR-505-5p reversed regulatory effects of MIAT on VSMCs phenotypes. LncRNA\n MIAT stimulates VSMCs in hypertension mice to proliferate and migrate through downregulating miR-505-5p, which may be a promising target for diagnosis and treatment of hypertension.","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":"25 22","pages":""},"PeriodicalIF":4.7000,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"5","ListUrlMain":"https://doi.org/10.1166/jbn.2024.3824","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

To clarify the role of long non-coding RNA (lncRNA) MIAT in regulating proliferative and migratory abilities in VSMCs extracted from hypertension mice via downregulating microRNA-505-5p (miR-505-5p). Serum levels of MIAT and miR-505-5p in enrolled 20 hypertension patients and 20 healthy volunteers were detected. VSMCs were extracted from hypertension mice and healthy mice. Regulatory effects of MIAT and miR-505-5p on proliferative and migratory abilities in VSMCs were examined. At last, the interaction between MIAT and miR-505-5p was explored by dual-luciferase reporter assay and rescue experiments. Serum level of MIAT was higher in hypertension patients than those of healthy subjects, while miR-505-5p was downregulated. MIAT level was negatively correlated to miR-505-5p level in serum of hypertension patients. Knockdown of MIAT suppressed proliferative and migratory abilities in VSMCs extracted from hypertension mice. In addition, knockdown of MIAT upregulated E-cadherin and downregulated Vimentin and Snail-1. MiR-505-5p was verified to be the target binding MIAT. Knockdown of miR-505-5p reversed regulatory effects of MIAT on VSMCs phenotypes. LncRNA MIAT stimulates VSMCs in hypertension mice to proliferate and migrate through downregulating miR-505-5p, which may be a promising target for diagnosis and treatment of hypertension.
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
LncRNA 心肌梗死相关转录本 (MIAT)/miR-505-5p 轴调控高血压小鼠血管平滑肌细胞的增殖和迁移
目的:阐明长非编码 RNA(lncRNA)MIAT 通过下调 microRNA-505-5p (miR-505-5p)调节高血压小鼠血管内皮细胞增殖和迁移能力的作用。检测了 20 名高血压患者和 20 名健康志愿者血清中 MIAT 和 miR-505-5p 的水平。提取了高血压小鼠和健康小鼠的血管内皮细胞。研究了 MIAT 和 miR-505-5p 对血管内皮细胞增殖和迁移能力的调控作用。最后,通过双荧光素酶报告实验和拯救实验探讨了 MIAT 和 miR-505-5p 之间的相互作用。结果发现,高血压患者血清中的 MIAT 水平高于健康人,而 miR-505-5p 则出现下调。高血压患者血清中 MIAT 的水平与 miR-505-5p 的水平呈负相关。敲除 MIAT 可抑制高血压小鼠血管内皮细胞的增殖和迁移能力。此外,敲除 MIAT 会上调 E-cadherin,下调 Vimentin 和 Snail-1。MiR-505-5p 被证实是结合 MIAT 的靶标。敲除 miR-505-5p 逆转了 MIAT 对 VSMC 表型的调控作用。LncRNA MIAT通过下调miR-505-5p刺激高血压小鼠的VSMC增殖和迁移,这可能是诊断和治疗高血压的一个有前景的靶点。
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
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
期刊介绍: ACS Applied Bio Materials is an interdisciplinary journal publishing original research covering all aspects of biomaterials and biointerfaces including and beyond the traditional biosensing, biomedical and therapeutic applications. The journal is devoted to reports of new and original experimental and theoretical research of an applied nature that integrates knowledge in the areas of materials, engineering, physics, bioscience, and chemistry into important bio applications. The journal is specifically interested in work that addresses the relationship between structure and function and assesses the stability and degradation of materials under relevant environmental and biological conditions.
期刊最新文献
Issue Publication Information Issue Editorial Masthead Architecture-Driven Preclinical Bone Regeneration in 3D-Printed Hydroxyapatite Scaffolds with Local Nanomechanical Insights Core−Shell Electrospun Membranes Enable Antimicrobial and Immunomodulatory Local Therapy for Periodontitis 12-Hydroxylauric Acid-Tethered Heterochiral Diphenylalanines: A Promising Antimicrobial Peptide Scaffold for In Vivo Wound Healing Applications
×
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学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:604180095
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