Moreno Alexa, Alarcón-Zapata Pedro, Guzmán-Gútierrez Enrique, Radojkovic Claudia, Contreras Héctor, Nova-Lampeti Estefanía, A Zúñiga Felipe, Rodriguez-Alvárez Llerenty, Escudero Carlos, Lagos Paola, Aguayo Claudio
Department of Clinical Biochemistry and Immunology, Faculty of Pharmacy, University of Concepcion, P.O. Box 237, Concepción 4030000, Chile.
Clinical Laboratory Program, Faculty of Health Sciences, State University of Southern Manabí, Jipijapa 130402, Ecuador.
Biomedicines. 2024 Sep 18;12(9):2119. doi: 10.3390/biomedicines12092119.
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.
急性心肌梗死（AMI）由易损斑块破裂引起，导致缺血性心肌细胞坏死和强烈炎症反应。矛盾的是，这种炎症会释放有助于心脏修复的因子。最近的研究结果表明，细胞外囊泡（EVs）在急性心肌梗死后心脏修复过程中的细胞间通讯中发挥作用。然而，急性心肌梗死患者血液中EVs的组织来源和趋化因子谱仍不清楚。本研究对急性心肌梗死患者冠状动脉血和外周血中EVs的组织来源和趋化因子受体谱进行了表征。结果显示，从冠状动脉血浆和外周血浆中分离出的囊泡富含四跨膜蛋白（CD9），并表达CD81、CD90和CD144。囊泡大小在145至162纳米之间，对照组的囊泡（D10）比急性心肌梗死组的小。此外，所有囊泡均表达CCR6和CXCR3，而一小部分表达CCR4。另外，与对照组相比，急性心肌梗死患者冠状动脉血和外周血中的囊泡CXCR3和CCR6表达降低；然而，急性心肌梗死患者冠状动脉血和外周血中的囊泡之间未发现差异。总之，我们的研究首次证明了急性心肌梗死患者外周循环中表达CD144、CXCR3和CCR6的细胞外囊泡数量的变化。急性心肌梗死患者循环中的细胞外囊泡作为一种潜在的诊断工具具有很好的前景。
