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Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease
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Digital PCR for Quantifying Circulating MicroRNAs in Acute Myocardial Infarction and Cardiovascular Disease

Published on: July 3, 2018

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Circulating miR-379 as a potential novel biomarker for diagnosis of acute myocardial infarction

J Yi1, Y An

  • 1Department of General Ward, Community Health Service Center of Laoshan District, Qingdao, Shandong, China; Medical College of Qingdao University, Qingdao, Shandong, China. ylianghuang@yeah.net.

European Review for Medical and Pharmacological Sciences
|February 10, 2018
PubMed
Abstract

Insights

Plasma miR-379 levels are decreased in acute myocardial infarction (AMI) patients. This microRNA may serve as a novel biomarker for early AMI diagnosis by influencing vascular smooth muscle cell function.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiology

Background:

  • MicroRNA-379 (miR-379) is implicated in cell proliferation.
  • Acute myocardial infarction (AMI) diagnosis requires reliable biomarkers.

Purpose of the Study:

  • To investigate the role of miR-379 in AMI diagnosis.
  • To assess miR-379's diagnostic potential and functional impact on vascular smooth muscle cells (VSMCs).

Main Methods:

  • Quantitative Real-time PCR (qRT-PCR) to measure plasma miR-379 levels in AMI patients and healthy controls.
  • Receiver-operator characteristic (ROC) analysis to evaluate diagnostic accuracy.
  • In vitro assays (CCK-8, flow cytometry) to assess VSMC proliferation and cell cycle.

Main Results:

  • Plasma miR-379 levels were significantly lower in AMI patients compared to controls.
  • miR-379 levels negatively correlated with cardiac biomarkers CK-MB and cTn.
  • ROC analysis showed an AUC of 0.751 for AMI discrimination.
  • miR-379 inhibited VSMC proliferation and induced G0/G1 cell cycle arrest.

Conclusions:

  • miR-379 shows potential as a novel biomarker for early AMI diagnosis.
  • The mechanism involves miR-379's effect on VSMC proliferation and cell cycle regulation.

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