Extracellular vesicles from monocyte/platelet aggregates modulate human atherosclerotic plaque reactivity
Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF‐α display pro‐inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering...
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| Published in: | Journal of extracellular vesicles Vol. 10; no. 6; pp. 12084 - n/a |
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| Main Authors: | , , , , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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John Wiley & Sons, Inc
01-04-2021
John Wiley and Sons Inc Wiley |
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| Abstract | Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF‐α display pro‐inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering platelet activation with Iloprost, Aspirin or a P2Y12 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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| AbstractList | Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF‐α display pro‐inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering platelet activation with Iloprost, Aspirin or a P2Y12 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. Abstract Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF‐α display pro‐inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering platelet activation with Iloprost, Aspirin or a P2Y12 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. Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF‐α display pro‐inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering platelet activation with Iloprost, Aspirin or a P2Y 12 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. Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates of monocytes and platelets in response to TNF-α display pro-inflammatory actions on endothelial cells and atherosclerotic plaques. Tempering platelet activation with Iloprost, Aspirin or a P2Y 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. |
| Author | Marcone, Simone Fitzsimons, Stephen Montero‐Melendez, Trinidad Godson, Catherine Oggero, Silvia Cooper, Dianne Burgoyne, Thomas Perretti, Mauro Gaetano, Monica Barry, Mary Pinto, Andreia L. Ikramova, Dinara Belton, Orina Burke, David Brennan, Eoin P. Norling, Lucy V. |
| AuthorAffiliation | 2 Diabetes Complications Research Centre Conway Institute, & School of Medicine University College Dublin Dublin Ireland 4 Royal Brompton & Harefield NHS Foundation Trust London UK 6 Department of Vascular Surgery St. Vincent's University Hospital Dublin Ireland 1 William Harvey Research Institute Bart's and the London School of Medicine Queen Mary University of London London UK 3 Trinity Translational Medicine Institute Trinity College Dublin Dublin Ireland 8 Institute of Ophthalmology, Faculty of Brain Sciences University College London London UK 5 School of Engineering and Materials Science Queen Mary University of London London UK 7 Centre for inflammation and Therapeutic Innovation Queen Mary University of London London UK |
| AuthorAffiliation_xml | – name: 1 William Harvey Research Institute Bart's and the London School of Medicine Queen Mary University of London London UK – name: 5 School of Engineering and Materials Science Queen Mary University of London London UK – name: 3 Trinity Translational Medicine Institute Trinity College Dublin Dublin Ireland – name: 7 Centre for inflammation and Therapeutic Innovation Queen Mary University of London London UK – name: 4 Royal Brompton & Harefield NHS Foundation Trust London UK – name: 6 Department of Vascular Surgery St. Vincent's University Hospital Dublin Ireland – name: 8 Institute of Ophthalmology, Faculty of Brain Sciences University College London London UK – name: 2 Diabetes Complications Research Centre Conway Institute, & School of Medicine University College Dublin Dublin Ireland |
| Author_xml | – sequence: 1 givenname: Silvia orcidid: 0000-0003-1451-3870 surname: Oggero fullname: Oggero, Silvia organization: Queen Mary University of London – sequence: 2 givenname: Monica orcidid: 0000-0002-4677-1447 surname: Gaetano fullname: Gaetano, Monica organization: Conway Institute, & School of Medicine University College Dublin – sequence: 3 givenname: Simone orcidid: 0000-0001-5516-4000 surname: Marcone fullname: Marcone, Simone organization: Trinity College Dublin – sequence: 4 givenname: Stephen surname: Fitzsimons fullname: Fitzsimons, Stephen organization: Conway Institute, & School of Medicine University College Dublin – sequence: 5 givenname: Andreia L. surname: Pinto fullname: Pinto, Andreia L. organization: Royal Brompton & Harefield NHS Foundation Trust – sequence: 6 givenname: Dinara surname: Ikramova fullname: Ikramova, Dinara organization: Queen Mary University of London – sequence: 7 givenname: Mary orcidid: 0000-0003-3780-5702 surname: Barry fullname: Barry, Mary organization: St. Vincent's University Hospital – sequence: 8 givenname: David surname: Burke fullname: Burke, David organization: St. Vincent's University Hospital – sequence: 9 givenname: Trinidad orcidid: 0000-0002-3563-376X surname: Montero‐Melendez fullname: Montero‐Melendez, Trinidad organization: Queen Mary University of London – sequence: 10 givenname: Dianne orcidid: 0000-0002-5553-9447 surname: Cooper fullname: Cooper, Dianne organization: Queen Mary University of London – sequence: 11 givenname: Thomas orcidid: 0000-0002-8428-720X surname: Burgoyne fullname: Burgoyne, Thomas organization: University College London – sequence: 12 givenname: Orina surname: Belton fullname: Belton, Orina organization: Conway Institute, & School of Medicine University College Dublin – sequence: 13 givenname: Lucy V. orcidid: 0000-0001-5316-9115 surname: Norling fullname: Norling, Lucy V. organization: Queen Mary University of London – sequence: 14 givenname: Eoin P. orcidid: 0000-0003-4908-5474 surname: Brennan fullname: Brennan, Eoin P. organization: Conway Institute, & School of Medicine University College Dublin – sequence: 15 givenname: Catherine orcidid: 0000-0003-0655-1041 surname: Godson fullname: Godson, Catherine organization: Conway Institute, & School of Medicine University College Dublin – sequence: 16 givenname: Mauro orcidid: 0000-0003-2068-3331 surname: Perretti fullname: Perretti, Mauro email: m.perretti@qmul.ac.uk organization: Queen Mary University of London |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33936566$$D View this record in MEDLINE/PubMed |
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| Snippet | Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed aggregates... Abstract Extracellular vesicles (EVs) are emerging as key players in different stages of atherosclerosis. Here we provide evidence that EVs released by mixed... |
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| SubjectTerms | Arteriosclerosis Aspirin Aspirin - pharmacology Atherosclerosis Atherosclerosis - physiopathology Blood platelets Blood Platelets - cytology Blood Platelets - drug effects Cardiovascular disease Cell activation Cloning Coronary artery disease Cytokines Endothelial cells Endothelial Cells - drug effects Explants Extracellular vesicles Extracellular Vesicles - drug effects Extracellular Vesicles - metabolism Extracellular Vesicles - physiology Gelsolin Healthy Volunteers Heart diseases Humans Inflammation Inflammation - immunology Leukocytes monocyte/platelet aggregates Monocytes Monocytes - cytology Monocytes - physiology Phenotypes Plaque, Atherosclerotic - physiopathology Plasma Platelet Activation - drug effects Platelet Aggregation - physiology Platelets Proteomics Tumor Necrosis Factor-alpha Tumor necrosis factor-TNF vascular inflammation |
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| Title | Extracellular vesicles from monocyte/platelet aggregates modulate human atherosclerotic plaque reactivity |
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