Fig. 6

Reduced cardiac dedifferentiation and reparative activity as IL-6 expression was genetically lacking in ADSC. A Immunostaining of cardiac troponin T (cTnT) revealed significant formation of dedifferential cardiomyocytes typically exhibited marginalization of cTnT protein in hearts treated with either wildtype ADSC (ADSC^WT) or ADSC lacking IL-6 production (ADSC^IL-6KO). B Quantitative comparison illustrated that ADSC^IL-6KO-injection (n = 6) yielded less than half counts of dedifferentiated cardiomyocytes (dedi-CM) found in the ADSC^WT-treated hearts (n = 4). C Representative H&E staining of MI heart at the mid-ventricular level illustrated an increase in wall thickness after injection of wildtype ADSC (MI + ADSC^WT, indicated by arrow), which was diminished as ADSC lacking IL-6 expression (ADSC^IL-6KO). D Quantitative analysis showed ADSC^IL-6KO treatment (n = 4) created less increase in ventricular wall thickness in comparison to the ADSC^WT injected hearts (n = 4). E A similar tendency of cardiomyocytes intensity (CM intensity) to wall thickness was found between two groups (n = 4 and 5, respectively). F Improvement of cardiac ejection fraction (EF measured by Millar catheter) in mice treated with ADSC^WT (n = 5) was significantly diminished in the ADSC^IL-6KO-treated mice (n = 5). *p < 0.05, **p < 0.01