Cardiomyocyte Exosomal Nanovesicles Mediating p53 to Regulate Autophagy and Protect Myocardial Infarction

This study explores the protective mechanism of cardiomyocyte exosome nanovesicles on myocardial infarction. Enzyme activity was measured and apoptosis of rat cardiomyocytes was assessed by TdT-mediated dUTP Nick-End Labeling (TUNEL) along with analysis of myocardial function by color Doppler echocardiogram. In addition, triphenyl tetrazolium chloride (TTC) staining evaluated the myocardial ischemia. BMSCs were co-cultured with primary cardiomyocytes followed by measuring autophagy and exosome morphology of myocardial tissue by transmission electron microscope and protein expression by Western blot. Exosomes secreted by Bone marrow mesenchymal stem cells (BMSCs) were successfully isolated. LDH, CK, CK-MB activity, cardiomyocyte apoptosis rate, LVESD, LVEDD, LVEDP, myocardial infarction area, cell area occupied by autophagic vesicles and p53 expression in model group were higher than control group (P < 0.05) and they were lower in exosome group than model group. In addition, LVEF, LVFS, and LVSP were lower in model IP 203.8.109.10 O F , 15 S p 2023 22 2944 group and higher in exosome group (P < 0.05). Model group showed significantly promoted autophagy activation and Copyright Ame ican Scentific Publishers autophagosome formation, which were inhibited bycardiomyocyte exosomes. Moreover, exosome-like vesicles were found Delivered by Ingenta with a diameter of 60-90 nm. Furthermore, PKH-26 staining showed that cardiomyocytes could uptake exosomes well. Myocardial injury significantly promotes autophagy activation. Moreover, the apoptosis rate of cardiomyocytes and the area of myocardial ischemia were reduced and the cardiac function of rats with myocardial infarction was improved.