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In Vivo Nanovector Delivery of a Heart-specific MicroRNA-sponge
Published on: June 15, 2018
miR-23 regulate the pathogenesis of patients with coronary artery disease
Yunfeng Di1, Dayong Zhang1, Teng Hu1
1Department of Cardiology, Sichuan Mianyang 404 Hospital (The Second Affiliated Hospital of North Sichuan Medical College) Sichuan, China.
Insights
Circulating miR-23 is elevated in coronary artery disease (CAD) patients and suppresses vascular endothelial growth factor (VEGF) and endothelial progenitor cell activity. This suggests miR-23 may serve as a diagnostic biomarker for CAD severity.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomarker Discovery
Background:
- Coronary artery disease (CAD) poses a significant global health challenge.
- Identifying novel biomarkers for CAD diagnosis and progression is crucial.
- The role of microRNAs (miRNAs) in cardiovascular disease pathogenesis is an emerging area of research.
Purpose of the Study:
- To investigate the expression of miR-23 in patients with coronary artery disease.
- To elucidate the mechanism by which miR-23 influences CAD progression.
- To evaluate the potential of miR-23 as a diagnostic biomarker for CAD.
Main Methods:
- Analysis of circulating miR-23 levels in three cohorts using real-time quantitative PCR.
- Assessment of the relationship between plasma miR-23 and coronary stenosis severity.
- In vitro and in vivo studies to determine the interaction between miR-23 and vascular endothelial growth factor (VEGF).
Main Results:
- miR-23 was found to be elevated in the plasma and diseased endothelial progenitor cells (EPCs) of CAD patients.
- miR-23 directly suppresses VEGF expression by binding to the 3'-UTR of VEGF mRNA.
- Suppression of miR-23 restored VEGF levels and angiogenic EPC activity, promoting blood flow recovery in ischemic limbs in mice.
Conclusions:
- Circulating miR-23 may serve as a novel biomarker for the diagnosis and severity assessment of CAD.
- miR-23's role in regulating VEGF and EPC function highlights its potential as a therapeutic target.
- Increased miR-23 levels correlate with the presence and severity of coronary lesions in CAD patients.
Objective:
To study whether miR-23 is regulated in coronary artery disease (CAD) patients and what is the possible mechanism of miR-23 in regulating CAD progression. Method Three different cohorts (including 13 AMI patients, 176 angina pectoris patients and 127 control subjects) were enrolled to investigate the expression levels of circulating miR-23 in patients with myocardial ischemia and also the relationship between plasma miR-23 and severity of coronary stenosis. Plasma miR-23 levels of participants were examined by real-time quantitative PCR. We further detected the correlation of miR-23 and VEGF by molecular and animal assays. Result miR-23 was enriched in not only diseased endothelial progenitor cells (EPCs) but also the plasma of CAD patients. Besides, we found out miR-23 was able to suppress VEGF expression and EPC activities. Reporter assays confirmed the direct binding and repression of miR-23 to the 3'-UTR of VEGF mRNA. Knock down of miR-23 not only restored VEGF levels and angiogenic activities of diseased EPCs in vitro, but further promoted blood flow recovery in ischemic limbs of mice. Conclusion Circulating miR-23 may be a new biomarker for CAD and as a potential diagnostic tool. And increased miR-23 level may be used to predict the presence and severity of coronary lesions in CAD patients.
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