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Platelets modulate cardiac remodeling via the collagen receptor GPVI after acute myocardial infarction

Friedrich Reusswig1, Matthias Dille1, E Krüger1

  • 1Department of Vascular- and Endovascular Surgery, University Hospital Düsseldorf, Heinrich-Heine University, Düsseldorf, Germany.

Frontiers in Immunology
|January 26, 2024
PubMed

Insights

Glycoprotein VI (GPVI) deficiency in mice improves cardiac remodeling after myocardial infarction by reducing platelet activation and altering scar collagen. This suggests GPVI is a therapeutic target for improving heart healing post-ischemia reperfusion injury.

Area of Science:

  • Cardiovascular Biology
  • Platelet Physiology
  • Immunology

Background:

  • Platelets are crucial in cardiovascular diseases, with enhanced activation post-myocardial infarction.
  • Platelet glycoprotein VI (GPVI) is a key collagen receptor involved in platelet activation and thrombus stability.
  • Previous studies suggested GPVI's role in inflammation and infarct size reduction, but its precise function in cardiac remodeling remained unclear.

Purpose of the Study:

  • To investigate the role of GPVI in cardiac remodeling and function following experimental acute myocardial infarction (AMI).
  • To determine if GPVI deficiency impacts inflammation, pro-coagulant activity, and scar formation post-AMI.

Main Methods:

  • Utilized GPVI-deficient mice in a closed-chest model of experimental AMI.
  • Analyzed inflammatory responses, platelet activation via GPVI and PAR4 receptor stimulation, and pro-coagulant activity.
  • Assessed plasma levels of TGF-β and gene expression related to cardiac remodeling (Col1a1, Col3a1, periostin, Cthrc1) at 7 days post-AMI.
  • Evaluated scar collagen quality and cardiac function at 21 days post-AMI.

Main Results:

  • GPVI deficiency did not significantly affect the inflammatory response in experimental AMI.
  • Reduced platelet activation in GPVI-deficient mice led to decreased pro-coagulant activity.
  • GPVI deficiency resulted in reduced plasma TGF-β levels and altered expression of cardiac remodeling genes.
  • Scar collagen quality improved, characterized by tighter, less fine collagen, leading to enhanced cardiac function in GPVI-deficient mice.

Conclusions:

  • GPVI is identified as a significant regulator of platelet-induced cardiac remodeling post-AMI.
  • Targeting GPVI may offer a therapeutic strategy to mitigate ischemia reperfusion injury and promote cardiac healing.
Abstract

Keywords:
glycoprotein VIinflammationmyocardial infarctionplateletsremodelingscar formation

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