PURPOSE: The purpose of this study was to detect and follow transplanted superparamagnetic iron oxide (SPIO)-labeled endothelial progenitor cells (EPCs) by magnetic resonance imaging (MRI). PROCEDURES: Infarcted rats were randomized to injections of SPIO-labeled EPCs, unlabeled EPCs, or saline. From 1 day to 8 weeks, in vivo serial MRI was performed for cell tracking. RESULTS: Labeled cells were visualized as hypointense areas by MRI. The presence of labeled EPCs at 10 days and disappearance of these cells by 8 weeks was confirmed by iron and 4',6-diamidino-2-phenylindole. Co-staining for iron and ED-1 showed that the iron-positive cells were macrophages. EPC implantation significantly elevated vascular endothelial growth factor expression, accompanied by increased capillary and arteriole density in the ischemic myocardium. CONCLUSIONS: At 8 weeks, the transplanted EPCs were not present and the enhanced MRI signals arose from macrophages. However, both EPCs enhanced cardiac function. The major mechanism of cardiac improvement appears to be paracrine pathways of the engrafted EPCs.
PURPOSE: The purpose of this study was to detect and follow transplanted superparamagnetic iron oxide (SPIO)-labeled endothelial progenitor cells (EPCs) by magnetic resonance imaging (MRI). PROCEDURES: Infarcted rats were randomized to injections of SPIO-labeled EPCs, unlabeled EPCs, or saline. From 1 day to 8 weeks, in vivo serial MRI was performed for cell tracking. RESULTS: Labeled cells were visualized as hypointense areas by MRI. The presence of labeled EPCs at 10 days and disappearance of these cells by 8 weeks was confirmed by iron and 4',6-diamidino-2-phenylindole. Co-staining for iron and ED-1 showed that the iron-positive cells were macrophages. EPC implantation significantly elevated vascular endothelial growth factor expression, accompanied by increased capillary and arteriole density in the ischemic myocardium. CONCLUSIONS: At 8 weeks, the transplanted EPCs were not present and the enhanced MRI signals arose from macrophages. However, both EPCs enhanced cardiac function. The major mechanism of cardiac improvement appears to be paracrine pathways of the engrafted EPCs.
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