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Updated: Jul 4, 2026
Non-invasive Assessment of Microvascular and Endothelial Function
Published on: January 29, 2013
[Circulating endothelial microparticles: a new marker of vascular injury]
C-M Boulanger1, A-S Leroyer, N Amabile
1Unité 689, centre de recherche cardiovasculaire, inserm Lariboisière, hôpital Lariboisière, 41, boulevard de la chapelle, 75475 Paris cedex 10, France. chantal.boulanger@larib.inserm.fr
Abstract:
Cell activation or apoptosis leads to plasma membrane blebbing and microparticles (MPs) release. MPs are submicron membrane vesicles expressing a panel of oxidized phospholipids and proteins specific of the cells they originate from. Exposure of negatively charged phospholipids and tissue factor confers a procoagulant potential to MPs. Increases in plasma MPs levels, particularly those of endothelial origin, reflects cellular injury and appears now as a surrogate marker of vascular dysfunction. MPs are also biologically active and stimulate pro-inflammatory responses in target cells. Thus, MPs can promote a prothrombogenic and pro-inflammatory vicious circle leading to vascular dysfunction. A better understanding of MPs composition, as well as their effects and the mechanisms leading to their clearance will likely open new therapeutic approaches in the treatment and the prognosis of cardiovascular diseases.
Insights
Cell activation releases microparticles (MPs), which are vesicles carrying cell-specific oxidized phospholipids and proteins. Elevated MPs, especially from endothelial cells, indicate vascular injury and dysfunction, promoting inflammation and thrombosis.
Area of Science:
- Biochemistry
- Cell Biology
- Cardiovascular Research
Background:
- Cell activation or apoptosis causes plasma membrane blebbing and microparticle (MP) release.
- MPs are vesicles carrying oxidized phospholipids and proteins specific to their cell of origin.
- MPs possess procoagulant potential due to exposed phospholipids and tissue factor.
Purpose of the Study:
- To investigate the role of MPs in vascular dysfunction.
- To understand the pro-inflammatory and prothrombotic effects of MPs.
- To explore therapeutic strategies targeting MPs in cardiovascular diseases.
Main Methods:
- Analysis of plasma MP levels, focusing on endothelial-derived MPs.
- Characterization of MP composition, including oxidized phospholipids and proteins.
- Assessment of MP biological activity on target cells, including inflammatory responses.
Main Results:
- Increased plasma MP levels, particularly endothelial MPs, correlate with cellular injury and vascular dysfunction.
- MPs exhibit procoagulant and pro-inflammatory properties.
- MPs contribute to a prothrombotic and pro-inflammatory cycle exacerbating vascular dysfunction.
Conclusions:
- MPs serve as a surrogate marker for vascular dysfunction and cellular injury.
- MPs actively promote a detrimental cycle of thrombosis and inflammation.
- Further understanding of MP biology and clearance mechanisms may yield new therapeutic targets for cardiovascular diseases.
