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Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
Published on: July 3, 2018
miR-3613-3p Is a New Diagnostic Indicator of Acute Coronary Syndrome (ACS) That Reduces Endothelial Damage by
Jianfei Liu1, Xiangran Wei2, Dongsheng Chen3
1Department of Cardiology, Institute of Cardiovascular Diseases, Xiangyang Central Hospital, Affiliated Hospital of Hubei University of Arts and Science, Xiangyang, Hubei, China.
Insights
This study identifies miR-3613-3p as a novel diagnostic biomarker for acute coronary syndrome (ACS). Lower miR-3613-3p levels in ACS patients alleviate endothelial injury by targeting RC3H1.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Biomarker Discovery
Background:
- Acute coronary syndrome (ACS) is a critical cardiovascular condition with significant morbidity and mortality.
- Endothelial injury plays a pivotal role in the pathogenesis of ACS.
- Novel diagnostic biomarkers and therapeutic targets for ACS are urgently needed.
Purpose of the Study:
- To investigate the diagnostic utility of miR-3613-3p in ACS.
- To elucidate the role of miR-3613-3p in hypoxia/reoxygenation (H/R)-induced endothelial injury.
- To identify the molecular mechanism underlying miR-3613-3p's function in ACS.
Main Methods:
- Quantitative real-time polymerase chain reaction (qRT-PCR) for miR-3613-3p expression.
- Receiver operator characteristic (ROC) curve and logistic regression for diagnostic assessment.
- In vitro assays (CCK-8, ELISA, oxidative stress markers) to evaluate endothelial cell injury.
- Dual-luciferase reporter assay to confirm target interaction (miR-3613-3p and RC3H1).
Main Results:
- Serum miR-3613-3p was significantly downregulated in ACS patients and correlated with clinical severity markers.
- miR-3613-3p overexpression protected human coronary artery endothelial cells (HCAECs) against H/R-induced injury, reducing inflammation and oxidative stress.
- RC3H1 was identified as a direct target of miR-3613-3p, and its overexpression reversed the protective effects of miR-3613-3p.
Conclusions:
- miR-3613-3p serves as a promising diagnostic biomarker for ACS.
- miR-3613-3p mitigates endothelial damage in ACS by targeting RC3H1.
- Targeting miR-3613-3p offers a potential therapeutic strategy for ACS intervention.
Abstract:
Focusing on acute coronary syndrome (ACS), a critical cardiovascular condition, this study explores the diagnostic utility of miR-3613-3p and its mechanistic involvement in endothelial injury. Quantitative real-time polymerase chain reaction (qRT-PCR) quantified serum and cell miR-3613-3p expression. Receiver operator characteristic (ROC) curve and logistic regression analysis assessed its diagnostic potential. Correlation analysis evaluated the association between miR-3613-3p and ACS. The effect of miR-3613-3p on hypoxia/reoxygenation (H/R)-induced human coronary artery endothelial cell (HCAEC) injury was evaluated by cell counting kit-8 (CCK-8, cell proliferation), enzyme linked immunosorbent assay (ELISA) kit (interleukin-6, IL-6; tumor necrosis factor-α, TNF-α), and commercialized assay kits (superoxide dismutase, SOD; glutathione, GSH, malonaldehyde, MDA). Dual-luciferase reporter assay validated the interaction between miR-3613-3p and ring finger and CCCH-type domains 1 (RC3H1). The recovery experiment assessed the effect of RC3H1 on H/R-induced HCAEC cell proliferation, inflammation, and oxidative stress. Compared to healthy individuals, serum miR-3613-3p in ACS, correlating with Gensini score, cardiac troponin I (cTnI), creatine kinase isoenzyme-MB (CK-MB), and left ventricular ejection fraction (LVEF), was downregulated and served as a diagnostic biomarker. In vitro, miR-3613-3p overexpression promoted cell proliferation, diminished inflammatory factor release, and reduced oxidative stress in H/R-induced HCAECs. RC3H1 was a direct target of miR-3613-3p, and its overexpression antagonized the cytoprotective influence of miR-3613-3p in H/R-induced HCAEC injury. miR-3613-3p is a novel biomarker for ACS and provides a new target for ACS intervention by alleviating endothelial damage via targeting RC3H1.
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