MiR-497-5p regulates ox-LDL-induced dysfunction in vascular endothelial cells by targeting VEGFA/p38/MAPK pathway in atherosclerosis
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View abstract on PubMed
Summary
This summary is machine-generated.MicroRNA-497-5p worsens endothelial cell dysfunction caused by oxidized LDL in atherosclerosis. It targets VEGFA, activating the p38/MAPK pathway and increasing apoptosis and inflammation.
Area Of Science
- Cardiovascular Biology
- Molecular Medicine
- Cellular Pathology
Background
- Oxidized low-density lipoprotein (ox-LDL) critically impairs endothelial cells, advancing atherosclerosis (AS).
- MiR-497-5p is a potential biomarker for AS, but its role in ox-LDL-induced endothelial dysfunction requires clarification.
Purpose Of The Study
- To investigate the role of miR-497-5p in ox-LDL-induced human umbilical vein endothelial cell (HUVEC) dysfunction.
- To elucidate the underlying molecular mechanisms involving VEGFA and the p38/MAPK pathway.
Main Methods
- Established an in vitro AS model using HUVECs exposed to ox-LDL.
- Assessed endothelial cell function (viability, apoptosis, inflammation, oxidative stress).
- Utilized quantitative real-time PCR, Western blot, and luciferase reporter assays to determine molecular mechanisms.
Main Results
- Ox-LDL upregulated miR-497-5p and p-p38, while downregulating VEGFA and p-eNOS in HUVECs.
- Ox-LDL exposure decreased HUVEC viability and angiogenesis, increasing apoptosis, inflammation, and oxidative stress, partly mediated by miR-497-5p.
- VEGFA was confirmed as a direct target of miR-497-5p; VEGFA interference reversed miR-497-5p silencing effects.
Conclusions
- MiR-497-5p exacerbates ox-LDL-induced endothelial dysfunction in HUVECs.
- This exacerbation occurs via targeting VEGFA and activating the p38/MAPK pathway.
- MiR-497-5p plays a significant role in the pathogenesis of ox-LDL-induced endothelial cell injury.
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