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Updated: Sep 11, 2025

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling
Published on: August 3, 2018
Silencing MMP2-AS1 inhibits the proliferation and migration of endothelial cells via YB-1
Zhetao Li1, Kuo Wang2, Ziliang Li3
1Heart Center, Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), Qingdao, China.
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.
Insights
Long noncoding RNA MMP2-AS1 promotes atherosclerosis by enhancing endothelial cell proliferation and migration via the YB-1 pathway. Targeting this MMP2-AS1/YB-1 axis may offer new atherosclerosis treatments.
Area of Science:
- Cardiovascular Biology
- Molecular Biology
- RNA Biology
Background:
- Endothelial cell proliferation and migration are crucial in atherosclerosis development.
- Long noncoding RNAs (lncRNAs) are implicated in atherosclerosis, affecting endothelial cell functions.
- The specific role of lncRNA matrix metalloproteinase 2 antisense RNA 1 (MMP2-AS1) in atherosclerosis is not fully understood.
Purpose of the Study:
- To investigate the molecular mechanism of lncRNA MMP2-AS1 in endothelial cells.
- To explore the role of the MMP2-AS1/YB-1 signaling pathway in atherosclerosis.
- To determine if MMP2-AS1 regulates human umbilical vein endothelial cell (HUVEC) proliferation and migration.
Main Methods:
- Established a HUVEC model using transforming growth factor-β1, oxidized low-density lipoprotein, and hypoxia.
- Measured the expression of lncRNA MMP2-AS1 under these conditions.
- Investigated the effect of MMP2-AS1 knockdown on HUVEC proliferation and migration, focusing on YB-1 interaction.
Main Results:
- Conditions mimicking atherosclerosis induced upregulation of lncRNA MMP2-AS1 expression in HUVECs.
- Knockdown of MMP2-AS1 significantly reduced HUVEC proliferation and migration.
- MMP2-AS1 was found to regulate HUVEC proliferation and migration by targeting YB-1.
Conclusions:
- The MMP2-AS1/YB-1 signaling pathway plays a significant role in regulating endothelial cell behavior in atherosclerosis.
- MMP2-AS1 promotes HUVEC proliferation and migration through YB-1 targeting.
- The MMP2-AS1/YB-1 axis represents a potential therapeutic target for treating atherosclerosis.
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