Cell therapy can boost cardiac function in animals and humans soon after injury, but the mechanism is unclear,. We performed cell treatment experiments in genetically engineered Myocardial Fms-like tyrosine kinase 3 (FLT-3)mice that permanently express green fluorescent protein (GFP) only in cardiomyocytas after a pulse of 4-OH-tamoxifen. Myocardial sellectchem infarction diluted the GFP(+) cardiomyocyte pool, indicating refreshment by non-GFP(+) progenitors. Cell therapy with bone marrow-derived c-kit(+) cells, but not mesenchymal stem cells, more diluted the GFP(+) pool, constant with c-kit(+) cell-mediated augmentation of cardiomyocyte progenitor action. This result could not be explained by transdifferentiation to cardiomyocytes by exogenously delivered c-kit(+) cells or by cell fusion. Treatment with c-kit(+) cells but riot mesenchymal stem cells enhanced cardiac function. These findings recommend that stimulation of endogenous cardiogenic progenitor exercise is really a vital mechanism ofMyocardial cardiac cell treatment.