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Published on: October 17, 2017
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Extracellular vesicles from monocyte/platelet aggregates modulate human atherosclerotic plaque reactivity
Silvia Oggero1, Monica de Gaetano2, Simone Marcone3
1William Harvey Research Institute Bart's and the London School of Medicine Queen Mary University of London London UK.
Journal of Extracellular Vesicles
|May 3, 2021
Summary
Extracellular vesicles (EVs) from activated monocytes and platelets promote atherosclerosis. Inhibiting platelet activation reduces their pro-inflammatory effects, suggesting a therapeutic target for cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Immunology
- Cell Biology
Background:
- Atherosclerosis involves complex cellular interactions, with extracellular vesicles (EVs) emerging as critical mediators.
- Monocyte-platelet aggregates are implicated in inflammatory processes within atherosclerotic plaques.
Purpose of the Study:
- To investigate the role of EVs released by monocyte-platelet aggregates in atherosclerosis.
- To determine if modulating platelet activation affects EV quantity, phenotype, and pro-inflammatory function.
- To explore the therapeutic potential of targeting these EVs in cardiovascular disease.
Main Methods:
- Stimulation of monocyte-platelet aggregates with TNF-α, with and without platelet inhibitors (Iloprost, Aspirin, P2Y12 inhibitor).
- Proteomic analysis of released EVs to identify compositional differences.
- Incubation of human atherosclerotic plaque explants with EVs to assess inflammatory cytokine release.
- Quantification of monocyte, platelet, and double-positive EV subsets in plasma from coronary artery disease patients.
Main Results:
- EVs from TNF-α-stimulated monocyte-platelet aggregates exhibited pro-inflammatory actions on endothelial cells and atherosclerotic plaques.
- Platelet inhibition altered EV quantity and phenotype, with distinct proteomic profiles (e.g., annexin-A1, gelsolin).
- EVs from Iloprost-treated aggregates induced minimal plaque activation compared to those from TNF-α alone.
- Elevated plasma levels of monocyte, platelet, and double-positive EVs were observed in patients with coronary artery disease.
Conclusions:
- EVs released by activated monocyte-platelet aggregates contribute to atherosclerosis development and progression.
- Modulating platelet activation impacts EV composition and function, offering a potential therapeutic strategy.
- Targeting the pro-inflammatory actions of these EVs may provide new avenues for atherosclerosis treatment.
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