A single dose of intravenous human amniotic membrane-derived mesenchymal stem cells limits transmural infarction, reduces fibrosis size, and improves left ventricular systolic function in the myocardial ischemic/reperfusion model of rats

Abstract

Despite the advances in coronary reperfusion in acute myocardial infarction (MI), post-MI heart failure is still a large burden of public health. Transmural infarction and extended fibrosis contribute largely to post-MI systolic dysfunction and heart failure, and thus cardioprotective strategies are crucial. Human amniotic membrane-derived mesenchymal stem cells (hAMSCs) have been shown with properties of immunomodulation, anti-inflammation, and low immunogenicity, which make them good candidates for cell therapies. In this study, a myocardial ischemia/reperfusion (I/R) model was established in rats, and hAMSCs were administered via the tail vein during coronary reperfusion. Compared to the control group, the rats receiving hAMSCs during the I/R procedure (hAMSC group) exhibited significantly better left ventricular ejection fractions after MI. Histological examinations of the hearts in hAMSC group showed minimal transmural infarction 4 weeks after the I/R procedure. Compared to the control group, hAMSC group had reduced size of cardiac fibrosis and less thinning of myocardial wall. In conclusion, intravenous hAMSCs limit transmural infarction, reduce fibrosis size, and improve left ventricular systolic function after MI in the animal model.