Trasplantation of Exosomes Derived From CD90 Positive Fibroblasts Reduce Apoptosis of Cardiomyocytes in Mice After Acute Myocardial Infarction

Abstract Myocardial infarction (MI) leads to cardiomyocyte death resulting in cardiac dysfunction. However, the molecular mechanism is still poorly understood. Cardiac fibroblasts can be marked by CD90, a N-glycosylated glycophosphatidylinositol anchored conserved cell surface protein, and the CD90 positive cardiac fibroblasts can release exosome against ischemic damage. Reduce apoptosis can promote the recovery of myocardial function after ischemic heart. Interestingly, exosome from CD90 positive cardiac fibroblasts can decrease the level of apoptosis after MI in vivo. However, the ability of CD90 positive cardiac fibroblasts exosome to reduce apoptosis, and the potential effects on the recovery of cardiomyocytes in heart after MI remain to be clarified. In this study, we found that CD90 positive cardiac fibroblasts exosome treated induced myocardial function recovery in a mouse MI model. Indeed, CD90 positive cardiac fibroblasts exosome increased phosphatidylinositol 3-kinase (PI3K) and kinase B (AKT) after MI. In addition, CD90 positive cardiac fibroblasts exosome decreased TUNEL in cardiomyocytes after MI. Furthermore, PI3K was inhibited by PI3K inhibitor LY294002, while hypoxia-stimulated primary cardiomyocytes were treated with CD90 positive cardiac fibroblasts exosome. Collectively, our results suggest that CD90 positive cardiac fibroblasts exosome can improve the recovery of cardiac function by decreasing apoptosis after MI in mice, likely via the PI3K/AKT signaling pathway.