{"title":"Silencing MMP2-AS1 inhibits the proliferation and migration of endothelial cells via YB-1.","authors":"Zhetao Li, Kuo Wang, Ziliang Li, Yifan Chi","doi":"10.1177/00368504251366369","DOIUrl":null,"url":null,"abstract":"<p><p><b>Objective:</b> The processes of proliferation and migration in endothelial cells are fundamental to the development of atherosclerosis. Recent studies underscore the critical involvement of long noncoding RNAs (lncRNAs) in atherosclerosis by influencing the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Nonetheless, the precise molecular mechanism of lncRNA matrix metalloproteinase 2 antisense RNA 1 (MMP2-AS1) remains inadequately characterized. <b>Methods:</b> To investigate this, we established a HUVEC model subjected to transforming growth factor-β1, oxidized low-density lipoprotein, and hypoxia, which resulted in the upregulation of lncRNA MMP2-AS1 expression. Further experimentation demonstrated that knockdown of MMP2-AS1 effectively mitigates the YB-1-mediated enhancement of HUVEC proliferation and migration. <b>Results:</b> Therefore, the primary aim of this research was to explore the role of the MMP2-AS1/YB-1 signaling pathway in atherosclerosis. The findings indicate that MMP2-AS1 regulates HUVEC proliferation and migration through YB-1 targeting. <b>Conclusions:</b> These results suggest that the MMP2-AS1/YB-1 axis holds potential as a therapeutic target for atherosclerosis treatment.</p>","PeriodicalId":56061,"journal":{"name":"Science Progress","volume":"108 3","pages":"368504251366369"},"PeriodicalIF":2.9000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12344352/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Science Progress","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1177/00368504251366369","RegionNum":4,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/8/12 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Objective: The processes of proliferation and migration in endothelial cells are fundamental to the development of atherosclerosis. Recent studies underscore the critical involvement of long noncoding RNAs (lncRNAs) in atherosclerosis by influencing the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Nonetheless, the precise molecular mechanism of lncRNA matrix metalloproteinase 2 antisense RNA 1 (MMP2-AS1) remains inadequately characterized. Methods: To investigate this, we established a HUVEC model subjected to transforming growth factor-β1, oxidized low-density lipoprotein, and hypoxia, which resulted in the upregulation of lncRNA MMP2-AS1 expression. Further experimentation demonstrated that knockdown of MMP2-AS1 effectively mitigates the YB-1-mediated enhancement of HUVEC proliferation and migration. Results: Therefore, the primary aim of this research was to explore the role of the MMP2-AS1/YB-1 signaling pathway in atherosclerosis. The findings indicate that MMP2-AS1 regulates HUVEC proliferation and migration through YB-1 targeting. Conclusions: These results suggest that the MMP2-AS1/YB-1 axis holds potential as a therapeutic target for atherosclerosis treatment.
期刊介绍:
Science Progress has for over 100 years been a highly regarded review publication in science, technology and medicine. Its objective is to excite the readers'' interest in areas with which they may not be fully familiar but which could facilitate their interest, or even activity, in a cognate field.