BACKGROUND: Cell transplantation therapy for heart failure is hindered by poor differentiation into cardiomyocytes and arrhythmias caused by the poor expression of connexin 43 (Cx43). A new stem cell source for cardiac regeneration is needed. METHODS AND RESULTS: Tongue muscle-derived Sca-1(+) cells (TDSCs) were isolated from normal and green fluorescence protein (GFP)-transgenic mouse tongues using surface antigen Sca-1. Cardiomyogenic differentiation was confirmed by measuring the calcium transient and the expression of cardiac-specific genes. The formation of gap junctions was confirmed by the expression of Cx43 and the dye transfer method. The contraction of regenerated cells was demonstrated by the calcium transients. GFP mouse-derived TDSCs were transplanted into hearts in a model of acute myocardial infarction. Three months after transplantation, LV remodeling was attenuated and the survival rate was improved compared with the control group. CONCLUSIONS: TDSCs form gap junctions and improve cardiac function and long-term survival after myocardial infarction.
BACKGROUND: Cell transplantation therapy for heart failure is hindered by poor differentiation into cardiomyocytes and arrhythmias caused by the poor expression of connexin 43 (Cx43). A new stem cell source for cardiac regeneration is needed. METHODS AND RESULTS: Tongue muscle-derived Sca-1(+) cells (TDSCs) were isolated from normal and green fluorescence protein (GFP)-transgenic mouse tongues using surface antigen Sca-1. Cardiomyogenic differentiation was confirmed by measuring the calcium transient and the expression of cardiac-specific genes. The formation of gap junctions was confirmed by the expression of Cx43 and the dye transfer method. The contraction of regenerated cells was demonstrated by the calcium transients. GFP mouse-derived TDSCs were transplanted into hearts in a model of acute myocardial infarction. Three months after transplantation, LV remodeling was attenuated and the survival rate was improved compared with the control group. CONCLUSIONS: TDSCs form gap junctions and improve cardiac function and long-term survival after myocardial infarction.