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Published on: June 15, 2018
Clinical Value and Potential Molecular Mechanism of miR-373-3p in Coronary Atherosclerosis
JiaYang Shen1, Lihong Tang2, Zhe Wang3
1School of Basic Medicine, Health Science Center, Yangtze University, Hubei, China.
Insights
MicroRNA-373-3p is elevated in coronary atherosclerosis (CAS) patients and acts as a risk factor. This microRNA inhibits endothelial progenitor cells, suggesting its role in CAS progression via VEGFA targeting.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Biomarker Discovery
Background:
- Coronary atherosclerosis (CAS) is a chronic inflammatory condition and the primary cause of coronary heart disease (CHD).
- Endothelial dysfunction, lipid accumulation, and fibrosis characterize CAS pathology.
Purpose of the Study:
- To investigate the clinical significance of miR-373-3p in carotid CAS.
- To elucidate the underlying mechanism of miR-373-3p in CAS progression.
Main Methods:
- Quantitative real-time PCR (RT-qPCR) to measure miR-373-3p expression in 95 CAS patients and 35 controls.
- ROC curve analysis for diagnostic value and logistic regression for risk factor assessment.
- In vitro studies using endothelial progenitor cells (EPCs) with miR-373-3p overexpression and knockdown.
Main Results:
- miR-373-3p levels were significantly higher in CAS patients compared to controls.
- miR-373-3p demonstrated diagnostic value for CAS and was identified as a risk factor.
- Overexpression of miR-373-3p inhibited EPC proliferation, migration, and invasion, while promoting apoptosis.
- miR-373-3p targets VEGFA, influencing CAS progression.
Conclusions:
- miR-373-3p serves as a sensitive biomarker for predicting CAS occurrence and progression.
- miR-373-3p plays a role in CAS pathogenesis by targeting VEGFA and affecting EPC function.
Abstract:
BackgroundCoronary atherosclerosis (CAS) is a chronic inflammatory condition marked by damage to the coronary artery endothelium, lipid accumulation, and fibrosis. It stands as the principal etiology of coronary heart disease (CHD).AimsThe rationale of this study was to investigate the clinical value and potential mechanism of miR-373-3p in carotid CAS.MethodsA total of 95 patients with CAS and 35 controls were enrolled in the study. RT-qPCR was used to evaluate the relative expression of miR-373-3p. ROC curve was used to analyze the diagnostic value of miR-373-3p in CAS. Logistic regression analysis was utilized to evaluate whether miR-373-3p serves as a risk factor for CAS. In addition, miR-373-3p overexpression and knockdown models of endothelial progenitor (EPCs) were established to investigate the mechanism of miR-373-3p in the regulation of EPCs.ResultsThe level of miR-373-3p in CAS patients was significantly increased. MiR-373-3p can well distinguish patients with CAS and is a risk factor for CAS. The over-expression of miR-373-3p can substantially inhibit the proliferation, migration and invasion of EPCs, and stimulate the apoptosis of EPCs. MiR-373-3p is involved in the progression of CAS by targeting VEGFA.ConclusionsAs a highly sensitive potential biomarker, miR-373-3p can predict the occurrence and progression of CAS. Additionally, miR-373-3p is involved in the progression of CAS by targeting VEGFA, which may play an essential role in the pathogenesis of CAS.
