Abstract
Exosomes are participated in the pathogenesis of cardiovascular diseases and can be secreted by mesenchymal stem cells (MSCs). However, the effects of circRNA, delivered by exosomes derived from MSCs, on myocardial injury remain unclear. Hence, this study aims to explore the therapeutic potential of exosomes derived from circRNA_0002113 lacking MSCs in the treatment of myocardial injury in vitro and in vivo. Our results reveal that exosomes derived from circRNA_0002113 lacking MSCs decreased cell apoptosis in anoxia-reoxygenation (A/R) model cells, and reduced myocardial injury by inhibiting nuclear translocation of RUNX1 in vitro and in vivo. Moreover, miR-188-3p, which targets RUNX1 in cardiomyocytes was also found to interact with circRNA_0002113. In conclusion, exosomes derived from circRNA_0002113 lacking MSCs could suppress myocardial infarction by sponging miR-188-3p to regulate RUNX1 nuclear translocation. The circRNA_0002113/miR-188-3p/RUNX1 axis mediated alleviation of apoptosis serves as a novel strategy to treat myocardial I/R injury.
Highlights
Myocardial infarction generally refers to myocardial necrosis caused by acute and persistent coronary ischemia (Osman et al, 2020)
The results indicate that treatment with both, pLVXcirc or exosomes isolated from pLVXcirc infected mesenchymal stem cells (MSCs) significantly decreased cell apoptosis when compared with the A/R control group (Figures 2H,I)
After treatment with pLVXcirc or exosomes isolated from pLVXcirc treated MSCs, RUNX1 nuclear translocation was found to be inhibited in A/R H9C2 cells (Figure 2J). These results suggest that exosomes derived from pLVXcirc treated MSCs suppressed RUNX1 nuclear translocation in A/R H9C2 cells
Summary
Myocardial infarction generally refers to myocardial necrosis caused by acute and persistent coronary ischemia (Osman et al, 2020). The primary clinical methods for treating myocardial infarction include drug therapy, coronary intervention, and coronary artery bypass grafting (Matteucci et al, 2019; Kupó et al, 2020). These measures can alleviate the initial myocardial damage in the acute phase, heart failure-derived cardiac remodeling negatively affects the treatment of patients with myocardial infarction (Tzahor and Poss, 2017; Bertero and Maack, 2018; Shah et al, 2019). Giricz et al found that ischemic preconditioning can induce secretion of exosomes, thereby making the myocardium resistant to a subsequent ischemic insult and reducing the area of myocardial infarction (Giricz et al, 2014)
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