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Int J Nanomedicine ; 15: 2647-2658, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-32368046

RESUMEN

PURPOSE: Myocardial ischemia-reperfusion injury primarily causes myocardial infarction (MI), which is manifested by cell death. Angiogenesis is essential for repair and regeneration in cardiac tissue after MI. In this study, we aimed to investigate the effect of exosomes derived from the serum of MI patients in angiogenesis and its related mechanism. PATIENTS AND METHODS: Exosomes, isolated from serum, were collected from MI (MI-exosome) and control (Con-exosome) patients. After coculturing with human umbilical vein endothelial cells, MI-exosome promoted cell proliferation, migration, and tube formation. RESULTS: The results revealed that the production and release of MI-exosome were associated with cardiomyocytes. Moreover, microarray assays demonstrated that miRNA-143 was significantly decreased in MI-exosome. Meanwhile, the overexpression and knockdown of miRNA-143 could inhibit and enhance angiogenesis, respectively. Furthermore, the effect of exosomal miRNA-143 on angiogenesis was mediated by its targeting gene, insulin-like growth factor 1 receptor (IGF-IR), and was associated with the production of nitric oxide (NO). CONCLUSION: Taken together, exosomes derived from the serum of patients with MI promoted angiogenesis through the IGF-IR/NO signaling pathway. The results provide novel understanding of the function of exosomes in MI.


Asunto(s)
Vasos Coronarios/metabolismo , Exosomas/metabolismo , MicroARNs/metabolismo , Infarto del Miocardio/sangre , Neovascularización Fisiológica , Receptor IGF Tipo 1/metabolismo , Animales , Línea Celular , Movimiento Celular , Proliferación Celular , Células Endoteliales de la Vena Umbilical Humana/metabolismo , Humanos , Masculino , Ratones Endogámicos C57BL , Ratones Desnudos , Óxido Nítrico/biosíntesis , Transducción de Señal
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