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Updated: May 12, 2026

Analysis of Extracellular Vesicle-Mediated Vascular Calcification Using In Vitro and In Vivo Models
09:01

Analysis of Extracellular Vesicle-Mediated Vascular Calcification Using In Vitro and In Vivo Models

Published on: January 27, 2023

Macrophage-derived matrix vesicles: an alternative novel mechanism for microcalcification in atherosclerotic plaques

Sophie E P New1, Claudia Goettsch, Masanori Aikawa

  • 1Center for Interdisciplinary Cardiovascular Sciences, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Circulation Research
|April 26, 2013
PubMed
Abstract

Insights

Macrophages release matrix vesicles (MVs) that contribute to microcalcification. These MVs, enriched in S100A9 and annexin V, accelerate calcification, particularly in chronic kidney disease.

Area of Science:

  • Cardiovascular Biology
  • Vascular Calcification
  • Macrophage Biology

Background:

  • Early atherosclerotic plaque calcification is linked to macrophage accumulation.
  • Chronic kidney disease and mineral imbalance accelerate calcification and matrix vesicle (MV) release.

Purpose of the Study:

  • To test the hypothesis that macrophage-derived MVs directly contribute to microcalcification.
  • Investigate the role of MVs in the pathogenesis of vascular calcification.

Main Methods:

  • Analysis of human carotid plaques for macrophage-associated calcified structures.
  • In vitro studies of macrophage-derived MV calcification potential.
  • Molecular analysis of MV contents (exosomal markers, S100A9, annexin V).
  • In vitro S100A9 silencing and in vivo S100A9 knockout mouse studies.
  • Investigation of the phosphatidylserine-annexin V-S100A9 complex in hydroxyapatite nucleation.

Main Results:

  • Macrophages were found in calcified regions of human plaques.
  • Macrophage-derived MVs exhibited high calcification and aggregation potential in vitro.
  • MVs contained exosomal markers, S100A9, and annexin V.
  • S100A9 silencing/deficiency reduced MV calcification; S100A9 stimulation increased it.
  • A phosphatidylserine-annexin V-S100A9 complex facilitates hydroxyapatite nucleation on MV membranes.

Conclusions:

  • Macrophages release calcifying MVs enriched in S100A9 and annexin V.
  • These MVs contribute to accelerated microcalcification.
  • Findings support a novel mechanism for MV-driven vascular calcification in chronic renal disease.
Keywords:
atherosclerosiscalcificationextracellular vesiclesinflammationmacrophagesrenal insufficiency, chronicrupture

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