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Platelet microparticles-containing miR-4306 inhibits human monocyte-derived macrophages migration through

Ying Yang1, Hui Luo2, Si Liu1

  • 1a Department of Cardiology , Affiliated Hospital of North Sichuan Medical College , Nanchong China.

Clinical and Experimental Hypertension (New York, N.Y. : 1993)
|September 6, 2018
PubMed

Insights

Platelet microparticles deliver miR-4306, a molecule downregulated in coronary artery disease (CAD). This transfer inhibits macrophage migration, suggesting a new therapeutic target for CAD and myocardial infarction.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biomarker Discovery

Background:

  • Platelets release microparticles (MPs) that mediate intercellular communication.
  • Platelet-secreted MPs (P-MPs) are implicated in various physiological and pathological processes.
  • MicroRNAs (miRNAs) are key regulators of gene expression and cellular function.

Purpose of the Study:

  • To investigate the role of microRNA-4306 (miR-4306) in coronary artery disease (CAD).
  • To determine the source and function of miR-4306 in the context of cardiovascular disease.
  • To explore the potential of P-MPs as carriers for therapeutic miRNAs.

Main Methods:

  • Quantification of miR-4306 expression in platelets and P-MPs from CAD patients.
  • Analysis of plasma miR-4306 localization (MPs, Argonaute2 complexes, HDL).
  • In vitro studies on human monocyte-derived macrophages (HMDMs) migration.
  • In vivo studies in a mouse model of myocardial infarction.

Main Results:

  • miR-4306 expression was downregulated in platelets and P-MPs of CAD patients.
  • Plasma miR-4306 primarily associated with MPs.
  • P-MPs delivered miR-4306 to HMDMs, inhibiting their migration in vitro.
  • miR-4306 reduced cardiac macrophage infiltration in mice with myocardial infarction.
  • The inhibitory effect of miR-4306 on HMDMs was mediated via VEGFA and the ERK/NF-κB signaling pathway.

Conclusions:

  • Platelet-derived miR-4306 is a potential prognostic biomarker for CAD.
  • Intercellular transfer of miR-4306 via P-MPs inhibits macrophage migration.
  • The VEGFA/ERK1/2/NF-κB signaling pathway mediates the anti-migratory effects of miR-4306.
  • P-MPs represent a promising delivery vehicle for miR-4306 in cardiovascular therapeutics.
Keywords:
Plateletcoronary artery diseasemiR-4306microparticlesvascular endothelial growth factor A

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