Changes in the Release of Endothelial Extracellular Vesicles CD144+, CCR6+, and CXCR3+ in Individuals with Acute
Alexa Moreno1,2, Pedro Alarcón-Zapata1, Enrique Guzmán-Gútierrez1
1Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, Chile.
Insights
Extracellular vesicles (EVs) in acute myocardial infarction (AMI) patients show altered expression of specific markers. These circulating EVs may serve as a novel diagnostic tool for AMI.
Area of Science:
- Cardiovascular Biology
- Cellular and Molecular Medicine
- Biomarker Discovery
Background:
- Acute myocardial infarction (AMI) involves cardiomyocyte necrosis and inflammation, with extracellular vesicles (EVs) implicated in cardiac repair.
- The precise origin and chemokine profile of EVs in AMI patients' circulation are not well understood.
Purpose of the Study:
- To characterize the tissue origin and chemokine receptor expression of EVs in coronary and peripheral blood of AMI patients.
- To investigate potential diagnostic applications of circulating EVs in AMI.
Main Methods:
- Isolation and characterization of EVs from coronary and peripheral blood plasma of AMI patients and controls.
- Analysis of EV surface markers (CD9, CD81, CD90, CD144) and chemokine receptors (CCR6, CXCR3, CCR4) via flow cytometry and size analysis.
Main Results:
- EVs from AMI patients' blood expressed CD9, CD81, CD90, and CD144, with larger vesicle sizes compared to controls.
- All EVs expressed CCR6 and CXCR3; a subset expressed CCR4.
- AMI-associated EVs showed decreased CXCR3 and CCR6 expression compared to controls, with no difference between coronary and peripheral blood.
Conclusions:
- Circulating EVs in AMI patients exhibit distinct characteristics, including altered CD144, CXCR3, and CCR6 expression.
- These findings highlight the potential of peripheral EVs as a diagnostic biomarker for acute myocardial infarction.
Abstract:
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+, CD90+, and CD144+. 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+, 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.
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