Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction
Acute myocardial infarction (AMI) results from vulnerable plaque rupture, causing ischemic cardiomyocyte necrosis and intense inflammation. Paradoxically, this inflammation releases factors that aid heart repair. Recent findings suggest a role for extracellular vesicles (EVs) in intercellular commun...
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MDPI AG
2024-09-01
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| Series: | Biomedicines |
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| Online Access: | https://www.mdpi.com/2227-9059/12/9/2119 |
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| author | Alexa Moreno Pedro Alarcón-Zapata Enrique Guzmán-Gútierrez Claudia Radojkovic Héctor Contreras Estefanía Nova-Lampeti Felipe A. Zúñiga Llerenty Rodriguez-Alvárez Carlos Escudero Paola Lagos Claudio Aguayo |
| author_facet | Alexa Moreno Pedro Alarcón-Zapata Enrique Guzmán-Gútierrez Claudia Radojkovic Héctor Contreras Estefanía Nova-Lampeti Felipe A. Zúñiga Llerenty Rodriguez-Alvárez Carlos Escudero Paola Lagos Claudio Aguayo |
| author_sort | Alexa Moreno |
| collection | DOAJ |
| description | Acute myocardial infarction (AMI) results from vulnerable plaque rupture, causing ischemic cardiomyocyte necrosis and intense inflammation. Paradoxically, this inflammation releases factors that aid heart repair. Recent findings suggest a role for extracellular vesicles (EVs) in intercellular communication during post-AMI cardiac repair. However, EVs’ tissue origin and chemokine profile in the blood of patients with AMI remains unclear. This study characterized the tissue origin and chemokine receptor profile of EVs in the coronary and peripheral blood of patients with AMI. The results reveal that vesicles isolated from coronary and peripheral blood plasma are enriched in tetraspanin (CD9) and express CD81<sup>+</sup>, CD90<sup>+</sup>, and CD144<sup>+</sup>. The vesicle size ranged between 145 and 162 nm, with the control group exhibiting smaller vesicles (D10) than the AMI group. Furthermore, all vesicles expressed CCR6 and CXCR3, whereas a small percentage expressed CCR4. In addition, a decrease in CXCR3 and CCR6 expression was observed in coronary and peripheral AMI blood vesicles compared with the control; however, no difference was found between AMI coronary and AMI peripheral blood vesicles. In conclusion, our study demonstrates, for the first time, changes in the number of extracellular vesicles expressing CD144<sup>+</sup>, CXCR3, and CCR6 in the peripheral circulation of patients with AMI. Extracellular vesicles present in the circulation of patients with AMI hold excellent promise as a potential diagnostic tool. |
| format | Article |
| id | doaj-art-2cd07d9125d548ce82291725f4e8785d |
| institution | OA Journals |
| issn | 2227-9059 |
| language | English |
| publishDate | 2024-09-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Biomedicines |
| spelling | doaj-art-2cd07d9125d548ce82291725f4e8785d2025-08-20T01:56:00ZengMDPI AGBiomedicines2227-90592024-09-01129211910.3390/biomedicines12092119Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial InfarctionAlexa Moreno0Pedro Alarcón-Zapata1Enrique Guzmán-Gútierrez2Claudia Radojkovic3Héctor Contreras4Estefanía Nova-Lampeti5Felipe A. Zúñiga6Llerenty Rodriguez-Alvárez7Carlos Escudero8Paola Lagos9Claudio Aguayo10Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Animal Science, Faculty of Veterinary Sciences, University of Concepcion, Chillán 3780000, ChileVascular Physiology Laboratory, Department of Basic Sciences, Universidad del Bio-Bio, Chillán 3780000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileDepartment of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, ChileAcute myocardial infarction (AMI) results from vulnerable plaque rupture, causing ischemic cardiomyocyte necrosis and intense inflammation. Paradoxically, this inflammation releases factors that aid heart repair. Recent findings suggest a role for extracellular vesicles (EVs) in intercellular communication during post-AMI cardiac repair. However, EVs’ tissue origin and chemokine profile in the blood of patients with AMI remains unclear. This study characterized the tissue origin and chemokine receptor profile of EVs in the coronary and peripheral blood of patients with AMI. The results reveal that vesicles isolated from coronary and peripheral blood plasma are enriched in tetraspanin (CD9) and express CD81<sup>+</sup>, CD90<sup>+</sup>, and CD144<sup>+</sup>. The vesicle size ranged between 145 and 162 nm, with the control group exhibiting smaller vesicles (D10) than the AMI group. Furthermore, all vesicles expressed CCR6 and CXCR3, whereas a small percentage expressed CCR4. In addition, a decrease in CXCR3 and CCR6 expression was observed in coronary and peripheral AMI blood vesicles compared with the control; however, no difference was found between AMI coronary and AMI peripheral blood vesicles. In conclusion, our study demonstrates, for the first time, changes in the number of extracellular vesicles expressing CD144<sup>+</sup>, CXCR3, and CCR6 in the peripheral circulation of patients with AMI. Extracellular vesicles present in the circulation of patients with AMI hold excellent promise as a potential diagnostic tool.https://www.mdpi.com/2227-9059/12/9/2119myocardial infarctionextracellular vesiclesCD144 |
| spellingShingle | Alexa Moreno Pedro Alarcón-Zapata Enrique Guzmán-Gútierrez Claudia Radojkovic Héctor Contreras Estefanía Nova-Lampeti Felipe A. Zúñiga Llerenty Rodriguez-Alvárez Carlos Escudero Paola Lagos Claudio Aguayo Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction Biomedicines myocardial infarction extracellular vesicles CD144 |
| title | Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction |
| title_full | Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction |
| title_fullStr | Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction |
| title_full_unstemmed | Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction |
| title_short | Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute Myocardial Infarction |
| title_sort | changes in the release of endothelial extracellular vesicles cd144 ccr6 and cxcr3 in individuals with acute myocardial infarction |
| topic | myocardial infarction extracellular vesicles CD144 |
| url | https://www.mdpi.com/2227-9059/12/9/2119 |
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