Circulating endothelial microparticles and miR-92a in acute myocardial infarction

Yuchen Zhang1, Junjun Cheng2, Fang Chen1

  • 1Department of Cardiology, Beijing An Zhen Hospital of the Capital University of Medical Sciences, Beijing 100029, China, Anzhen Road, Chaoyang District.

Bioscience Reports
|February 19, 2017
PubMed

Insights

Endothelial microparticles (EMPs) and miR-92a show diagnostic potential for acute myocardial infarction (AMI). Elevated levels of CD31+/CD42b- EMPs and miR-92a in AMI patients suggest their role in endothelial dysfunction.

Area of Science:

  • Cardiovascular Research
  • Biomarker Discovery
  • Endothelial Dysfunction

Background:

  • Coronary artery disease (CAD) involves endothelial dysfunction.
  • Microparticles (MPs) and microRNAs (miRNAs) are implicated in CAD pathogenesis.
  • Endothelial MPs (EMPs) and specific miRNAs may serve as diagnostic markers.

Purpose of the Study:

  • To evaluate the diagnostic utility of EMPs (CD31+/CD42b-) and miRNAs (miR-92a, miR-23a) in differentiating acute myocardial infarction (AMI) from stable CAD (SCAD).
  • To explore the correlation between EMPs and miRNA levels in AMI patients.
  • To assess the potential of these biomarkers in monitoring endothelial dysfunction in AMI.

Main Methods:

  • Plasma samples analyzed from 37 AMI patients, 42 SCAD patients, and 35 healthy controls.
  • Quantification of specific MP populations (CD31+/CD42b-, CD31+/CD42b+, CD31-/CD42b-) using flow cytometry.
  • Measurement of miR-92a and miR-23a levels via reverse transcription-quantitative PCR.
  • Cardiac troponin I (cTnI) measured by ELISA as a standard diagnostic parameter.

Main Results:

  • CD31+/CD42b- MP levels were significantly higher in the AMI group compared to SCAD and healthy groups.
  • miR-92a expression was significantly elevated in AMI patients relative to both SCAD and healthy groups.
  • A positive correlation was observed between CD31+/CD42b- MP levels and miR-92a expression.
  • Receiver operating characteristic (ROC) curve analysis showed high diagnostic accuracy for CD31+/CD42b- MPs (AUC=0.893), miR-92a (AUC=0.888), and cTnI (AUC=0.912).

Conclusions:

  • CD31+/CD42b- EMPs and miR-92a demonstrate significant potential as diagnostic biomarkers for AMI.
  • These biomarkers may aid in distinguishing AMI from stable CAD and reflect endothelial dysfunction.
  • Further investigation into their role in regulating endothelial dysfunction in AMI is warranted.

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