As the impairment of myocardial microenvironments due to coronary microembolization (CME) compromises the treatment effect of
percutaneous coronary intervention and leads to adverse prognosis, we hypothesized that endothelial progenitor cells (EPCs)
transplantation could improve cardiac function in the condition of CME. Low- (2 × 105) and high- (2 × 106) dose rat bone marrow-derived EPCs were transplanted in a model of CME. To develop a CME model, rats were injected with autologous micro-
blood-clots into the left ventricle. Echocardiograph was examined before and 1, 7, and 28 days after
EPC transplantation; serum cardiac
troponin I (cTNI),
von Willebrand factor (vWF), and cardiac
microRNA expression were examined one day after EPCs
transplantation. Heart morphology and
vascular endothelial growth factor (
VEGF), vWF, and
basic fibroblast growth factor (bFGF) expression were examined one day after
EPC transplantation. After 10 days of culture inductions, BM-EPCs have high purity as confirmed by flow cytometry. Cardiac function reflected by left ventricular ejection fraction significantly decreased after CME treatment and rescued by low-dose
EPC. Compared to the
sham group, cTNI and vWF serum levels increased significantly after CME treatment and rescued by low-dose
EPC and high-dose
EPC. Low-dose
EPC treatment decreased myocardial
necrosis and
fibrosis and elevated cardiac expression of
VEGF and vWF, while decreasing the cardiac expression of bFGF. Low-dose
EPC treatment significantly suppressed cardiac expression of microRNA-19a but significantly enhanced microRNA-21, microRNA-214, and microRNA-486-3p expression. In conclusion, our results indicate that low-dose
EPC transplantation may play a proangiogenic, antifibroblast, antifibrosis, and antinecrosis role and enhance cardiac function in a rat model of CME through a
microRNA-related pathway.