Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior
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 pro...
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MDPI AG
2022-04-01
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author | Marta Brambilla Maria Talmon Paola Canzano Luigia G. Fresu Sandra Brunelleschi Elena Tremoli Marina Camera |
author_facet | Marta Brambilla Maria Talmon Paola Canzano Luigia G. Fresu Sandra Brunelleschi Elena Tremoli Marina Camera |
author_sort | Marta Brambilla |
collection | DOAJ |
description | 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, <i>n</i> = 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, TNF<i>α</i>, 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, <i>n</i> = 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, TNF<i>α</i>, 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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spelling | doaj.art-de138b60eddf48a59e2e48ec830e5a892023-11-23T08:22:35ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-04-01239481110.3390/ijms23094811Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial BehaviorMarta Brambilla0Maria Talmon1Paola Canzano2Luigia G. Fresu3Sandra Brunelleschi4Elena Tremoli5Marina Camera6Centro Cardiologico Monzino, Istituto di Ricerca e Cura a Carattere Scientifico, 20138 Milan, ItalyDepartment of Health Sciences, School of Medicine, University of Piemonte Orientale, 28100 Novara, ItalyCentro Cardiologico Monzino, Istituto di Ricerca e Cura a Carattere Scientifico, 20138 Milan, ItalyDepartment of Health Sciences, School of Medicine, University of Piemonte Orientale, 28100 Novara, ItalyDepartment of Health Sciences, School of Medicine, University of Piemonte Orientale, 28100 Novara, ItalyMaria Cecilia Hospital, 48033 Cotignola, ItalyCentro Cardiologico Monzino, Istituto di Ricerca e Cura a Carattere Scientifico, 20138 Milan, ItalySeveral 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, <i>n</i> = 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, TNF<i>α</i>, 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, <i>n</i> = 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, TNF<i>α</i>, 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.https://www.mdpi.com/1422-0067/23/9/4811microvesiclesendothelial cellsmonocytesplateletscoronary artery disease |
spellingShingle | Marta Brambilla Maria Talmon Paola Canzano Luigia G. Fresu Sandra Brunelleschi Elena Tremoli Marina Camera Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior International Journal of Molecular Sciences microvesicles endothelial cells monocytes platelets coronary artery disease |
title | Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior |
title_full | Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior |
title_fullStr | Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior |
title_full_unstemmed | Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior |
title_short | Different Contribution of Monocyte- and Platelet-Derived Microvesicles to Endothelial Behavior |
title_sort | different contribution of monocyte and platelet derived microvesicles to endothelial behavior |
topic | microvesicles endothelial cells monocytes platelets coronary artery disease |
url | https://www.mdpi.com/1422-0067/23/9/4811 |
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