Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior |
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Authors: | Marta Brambilla Maria Talmon Paola Canzano Luigia G. Fresu Sandra Brunelleschi Elena Tremoli Marina Camera |
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Affiliation: | 1.Centro Cardiologico Monzino, Istituto di Ricerca e Cura a Carattere Scientifico, 20138 Milan, Italy; (M.B.); (P.C.);2.Department of Health Sciences, School of Medicine, University of Piemonte Orientale, 28100 Novara, Italy; (M.T.); (L.G.F.); (S.B.);3.Maria Cecilia Hospital, 48033 Cotignola, Italy;4.Department of Pharmaceutical Sciences, Università Degli Studi di Milano, 20133 Milan, Italy |
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Abstract: | Several contributions of circulating microvesicles (MVs) to the endothelial dysfunction have been reported in the past; a head-to-head comparison of platelet- and monocyte–derived MVs has however never been performed. To this aim, we assessed the involvement of these MVs in vessel damage related processes, i.e., oxidative stress, inflammation, and leukocyte-endothelial adhesion. Platelets and monocytes isolated from healthy subjects (HS, n = 15) were stimulated with TRAP-6 and LPS to release MVs that were added to human vascular endothelial cell (hECV) culture to evaluate superoxide anion production, inflammatory markers (IL-6, TNFα, NF-κB mRNA expression), and hECV adhesiveness. The effects of the MVs-induced from HS were compared to those induced by MVs spontaneously released from cells of patients with ST-segment elevation myocardial infarction (STEMI, n = 7). MVs released by HS-activated cells triggered a threefold increase in oxidative burst in a concentration-dependent manner. Only MVs released from monocytes doubled IL-6, TNFα, and NF-κB mRNA expression and monocyte-endothelial adhesion. Interestingly, the effects of the MVs isolated from STEMI-monocytes were not superimposable to previous ones except for adhesion to hECV. Conversely, MVs released from STEMI-platelets sustained both redox state and inflammatory phenotype. These data provide evidence that MVs released from activated and/or pathologic platelets and monocytes differently affect endothelial behavior, highlighting platelet-MVs as causative factors of impaired endothelial function in the acute phase of STEMI. |
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Keywords: | microvesicles endothelial cells monocytes platelets coronary artery disease |
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