下调 microRNA-221-3p 可通过靶向沉默信息调节因子 1 激活 RAF/MEK/ERK 信号通路,促进脂蛋白(a)损伤的内皮祖细胞的血管生成。

IF 3.4 3区 医学 Q2 MEDICINE, RESEARCH & EXPERIMENTAL
Molecular medicine reports Pub Date : 2024-12-01 Epub Date: 2024-10-04 DOI:10.3892/mmr.2024.13347
Xiaolei Zhang, Shizhen Wang, Yongting Qin, Hang Guo
{"title":"下调 microRNA-221-3p 可通过靶向沉默信息调节因子 1 激活 RAF/MEK/ERK 信号通路,促进脂蛋白(a)损伤的内皮祖细胞的血管生成。","authors":"Xiaolei Zhang, Shizhen Wang, Yongting Qin, Hang Guo","doi":"10.3892/mmr.2024.13347","DOIUrl":null,"url":null,"abstract":"<p><p>The present study aimed to investigate the role of microRNA (miR)‑221‑3p in endothelial progenitor cells (EPCs) treated with lipoprotein(a) [LP(a)]. EPCs were identified using immunofluorescence assays and miR‑221‑3p levels were measured using reverse transcription‑quantitative PCR. EPC migration was detected using Transwell assays, proliferation was measured by staining with 5‑ethynyl‑2'‑deoxyuridine and adhesion was assessed by microscopy. Flow cytometry was used to measure apoptosis and protein expression was detected using western blotting. A dual‑luciferase reporter assay was used to confirm the target interactions. The proliferation, migration, adhesion and angiogenesis of EPCs were decreased, and apoptosis was increased after treatment with LP(a). These effects were weakened by transfection with miR‑221‑3p inhibitor. The negative effects of LP(a) on EPCs were also weakened by overexpression of silent information regulator 1 (SIRT1). Inhibition of the RAF/MEK/ERK signaling pathway blocked the effects of SIRT1 overexpression. In conclusion, miR‑221‑3p inhibitor transfection activated the RAF/MEK/ERK signaling pathway through SIRT1, promoted the proliferation, migration, adhesion and angiogenesis of EPCs, and reduced apoptosis.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4000,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462396/pdf/","citationCount":"0","resultStr":"{\"title\":\"Downregulation of microRNA‑221‑3p promotes angiogenesis of lipoprotein(a)‑injured endothelial progenitor cells by targeting silent information regulator 1 to activate the RAF/MEK/ERK signaling pathway.\",\"authors\":\"Xiaolei Zhang, Shizhen Wang, Yongting Qin, Hang Guo\",\"doi\":\"10.3892/mmr.2024.13347\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>The present study aimed to investigate the role of microRNA (miR)‑221‑3p in endothelial progenitor cells (EPCs) treated with lipoprotein(a) [LP(a)]. EPCs were identified using immunofluorescence assays and miR‑221‑3p levels were measured using reverse transcription‑quantitative PCR. EPC migration was detected using Transwell assays, proliferation was measured by staining with 5‑ethynyl‑2'‑deoxyuridine and adhesion was assessed by microscopy. Flow cytometry was used to measure apoptosis and protein expression was detected using western blotting. A dual‑luciferase reporter assay was used to confirm the target interactions. The proliferation, migration, adhesion and angiogenesis of EPCs were decreased, and apoptosis was increased after treatment with LP(a). These effects were weakened by transfection with miR‑221‑3p inhibitor. The negative effects of LP(a) on EPCs were also weakened by overexpression of silent information regulator 1 (SIRT1). Inhibition of the RAF/MEK/ERK signaling pathway blocked the effects of SIRT1 overexpression. In conclusion, miR‑221‑3p inhibitor transfection activated the RAF/MEK/ERK signaling pathway through SIRT1, promoted the proliferation, migration, adhesion and angiogenesis of EPCs, and reduced apoptosis.</p>\",\"PeriodicalId\":18818,\"journal\":{\"name\":\"Molecular medicine reports\",\"volume\":\"30 6\",\"pages\":\"\"},\"PeriodicalIF\":3.4000,\"publicationDate\":\"2024-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462396/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Molecular medicine reports\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3892/mmr.2024.13347\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/10/4 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Molecular medicine reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3892/mmr.2024.13347","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/10/4 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

摘要

本研究旨在探讨微RNA(miR)-221-3p在经脂蛋白(a)[LP(a)]处理的内皮祖细胞(EPCs)中的作用。使用免疫荧光检测法鉴定 EPC,使用反转录定量 PCR 法测量 miR-221-3p 的水平。使用 Transwell 试验检测 EPC 迁移,用 5- 乙炔基-2'-脱氧尿苷染色测量增殖,用显微镜评估粘附。流式细胞术用于测量细胞凋亡,蛋白表达则通过 Western 印迹法检测。双荧光素酶报告实验用于确认目标相互作用。经 LP(a) 处理后,EPCs 的增殖、迁移、粘附和血管生成减少,凋亡增加。转染miR-221-3p抑制剂后,这些效应减弱。沉默信息调节因子1(SIRT1)的过表达也削弱了LP(a)对EPC的负面影响。抑制 RAF/MEK/ERK 信号通路可阻断 SIRT1 过表达的影响。总之,miR-221-3p抑制剂转染通过SIRT1激活了RAF/MEK/ERK信号通路,促进了EPCs的增殖、迁移、粘附和血管生成,并减少了细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Downregulation of microRNA‑221‑3p promotes angiogenesis of lipoprotein(a)‑injured endothelial progenitor cells by targeting silent information regulator 1 to activate the RAF/MEK/ERK signaling pathway.

The present study aimed to investigate the role of microRNA (miR)‑221‑3p in endothelial progenitor cells (EPCs) treated with lipoprotein(a) [LP(a)]. EPCs were identified using immunofluorescence assays and miR‑221‑3p levels were measured using reverse transcription‑quantitative PCR. EPC migration was detected using Transwell assays, proliferation was measured by staining with 5‑ethynyl‑2'‑deoxyuridine and adhesion was assessed by microscopy. Flow cytometry was used to measure apoptosis and protein expression was detected using western blotting. A dual‑luciferase reporter assay was used to confirm the target interactions. The proliferation, migration, adhesion and angiogenesis of EPCs were decreased, and apoptosis was increased after treatment with LP(a). These effects were weakened by transfection with miR‑221‑3p inhibitor. The negative effects of LP(a) on EPCs were also weakened by overexpression of silent information regulator 1 (SIRT1). Inhibition of the RAF/MEK/ERK signaling pathway blocked the effects of SIRT1 overexpression. In conclusion, miR‑221‑3p inhibitor transfection activated the RAF/MEK/ERK signaling pathway through SIRT1, promoted the proliferation, migration, adhesion and angiogenesis of EPCs, and reduced apoptosis.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Molecular medicine reports
Molecular medicine reports 医学-病理学
CiteScore
7.60
自引率
0.00%
发文量
321
审稿时长
1.5 months
期刊介绍: Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
×
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