Fig. 2
ADSCgfp+ subpopulation was more potent in cardiac structural repair and functional improvement. A Representative H&E staining at the mid-ventricular level showed a thin, fibrotic ventricular wall after myocardial infarction in the PBS-treated hearts (MI + PBS, n = 6), and injection of either ADSCgfp− (MI + ADSCgfp−, n = 5), or ADSCgfp+ (MI + ADSCgfp+, n = 6) cells mended the infarcted wall at the site of injection (arrows). Note that the ADSCgfp+ subset yielded more pronounced structural repair. Dotted line: wall thickness of non-infarcted hearts. B Identification of cardiomyocytes (CM) by immunostaining for cardiac Troponin T (cTnT) revealed almost doubled intensity of red fluorescence (CM) by ADSCgfp− injection (n = 5) and tripled in the ADSCgfp+ injected hearts (n = 6) in comparison to PBS controls (n = 6). C–F Cardiac contractile (dP/dtmax) and relaxing (dP/dtmin) properties, end-diastolic volume (EDV) and ejection fraction were derived from Millar catheter from three groups (n = 6, 5 and 6, respectively). Note that, injection of ADSCgfp+ cells significantly prevented the deterioration of cardiac function in PBS-treated MI hearts, while injection of ADSCgfp− cells only yielded tendentious but insignificant improvement of most cardiac parameters. *p < 0.05; **p < 0.01 compared to PBS control. #p < 0.05 compared to ADSCgfp−-treated hearts