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. 2016 Jun 22;5(8):1067–1078. doi: 10.5966/sctm.2015-0281

Figure 3.

Figure 3.

The mode of action of CPCs to ex vivo and in vivo ischemic heart. (A): Representative images of TUNEL-positive cells (green); nuclei were stained with DAPI (blue). NRVMs were labeled with an antibody against cardiac α-SA (white) (A1, A4, NRVM; A2, A5, NRVM + control-CPC; A3, A6; NRVM + APE1-CPC). Image magnification ×10. (B): Number of TUNEL-positive apoptotic NRVMs. Significantly decreased number of apoptotic NRVMs cocultured with APE1-CPCs compared with control-CPCs (n = 6, NRVM; n = 8, NRVM + control-CPC, NRVM + APE1-CPC) and increased number of TUNEL-positive apoptotic NRVMs cocultured with APE1-CPCs by E3330 exposure (n = 6). Percentage of apoptotic NRVMs, as evaluated by the TUNEL assay. (C): Quantitative analysis of the number of NRVMs after 3 days under anoxic conditions and decreased number of NRVMs cocultured with APE1-CPCs by E3330 exposure (n = 6). (D): CPC grafts in host ischemic hearts 7 days after injection. Representative micrographs of cardiac tissue sections in control-CPC (D1, D3) and APE1-CPC (D2, D4) mice (top: merged image of transplanted cells [red], cardiac α-sarcomeric actinin [green], and cell nuclei [blue]; bottom: transplanted cells [red] and cell nuclei [blue]). Image magnification ×20. (E): Number of DsRed-positive CPC grafts in total ischemic, infarct, and border areas of the host heart (n = 6 per group). ∗, p < .05. Abbreviations: APE1, apurinic/apyrimidinic endonuclease/redox factor 1; CPC, cardiac progenitor cell; Ct, control; DAPI, 4′,6-diamidino-2-phenylindole; NRVM, neonatal rat ventricular myocyte; SA, sarcomeric actinin; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling.