Demonstrates that extracellular vesicles from activated monocytes enhance plaque inflammation, indicating platelet inhibition alters vesicle composition to curb disease.
inhibitor impacted quantity and phenotype of EV produced. Proteomics of EVs from cells activated with TNF-α alone or in the presence of Iloprost revealed a distinct composition, with interesting hits like annexin-A1 and gelsolin. When added to human atherosclerotic plaque explants, EVs from TNF-α stimulated monocytes augmented release of cytokines. In contrast, EVs generated by TNF-α together with Iloprost produced minimal plaque activation. Notably, patients with coronary artery disease that required percutaneous coronary intervention had elevated plasma numbers of monocyte, platelet as well as double positive EV subsets. In conclusion, EVs released following monocyte/platelet activation may play a potential role in the development and progression of atherosclerosis. Whereas attenuating platelet activation modifies EV composition released from monocyte/platelet aggregates, curbing their pro-inflammatory actions may offer therapeutic avenues for the treatment of atherosclerosis.
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Oggero et al. (2021) studied this question.
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