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Related Experiment Video

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A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Complement factor C5a induces atherosclerotic plaque disruptions.

Anouk Wezel1, Margreet R de Vries, H Maxime Lagraauw

  • 1Division of Biopharmaceutics, Leiden Academic Centre for Drug Research, Leiden University, Leiden, The Netherlands; Department of Surgery, Leiden University Medical Center, Leiden, The Netherlands.

Journal of Cellular and Molecular Medicine
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PubMed
Summary

Complement factor C5a, a key part of the immune system, directly causes rupture in advanced atherosclerotic plaques. This occurs by increasing cell death within plaques, highlighting C5a signaling as a potential therapeutic target.

Keywords:
C5aapoptosisatherosclerosisplaque rupture

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Area of Science:

  • Immunology
  • Cardiovascular Biology
  • Pathology

Background:

  • Complement factor C5a (C5a) and its receptor C5aR are present in vulnerable atherosclerotic plaques.
  • A direct causal link between C5a and atherosclerotic plaque rupture remains unestablished.

Purpose of the Study:

  • To investigate the causal role of C5a in the rupture of advanced atherosclerotic plaques.
  • To explore the underlying mechanisms by which C5a may influence plaque instability.

Main Methods:

  • Accelerated atherosclerosis was induced in apoE(-/-) mice via vein grafts.
  • Local administration of C5a or PBS into established plaques.
  • In vitro studies on smooth muscle cells and endothelial cells treated with C5a.
  • Assessment of plaque morphology, disruption, hemorrhage, and apoptosis.

Main Results:

  • Local C5a treatment significantly increased C5aR expression within plaques.
  • C5a administration led to a marked increase in plaque disruptions and intraplaque hemorrhage.
  • In vitro, C5a induced significant apoptosis in smooth muscle and endothelial cells.
  • Apoptosis within the plaque was significantly elevated following C5a treatment in vivo.

Conclusions:

  • This study demonstrates a causal role for complement factor C5a in inducing atherosclerotic plaque disruptions.
  • C5a likely promotes plaque instability by inducing apoptosis in plaque-associated cells.
  • Targeting C5a signaling presents a promising strategy for preventing acute cardiovascular events stemming from plaque rupture.