A novel protective effect of erythropoietin in the infarcted heart
J. Clin. Invest. Cyrus J. Parsa, et al. 112:999 doi:10.1172/JCI18200 [Go to this article.]

Figure 2
Apoptotic cell death in H9c2 myoblasts exposed to oxidative stress and hypoxia. (a) The ratio of apoptotic cells to total adherent cells in the dish following oxidative stress (H₂O₂ exposure). Cells were treated with H₂O₂ (200 μM) following the treatment with EPO (0.4 or 10 U/ml, n = 8 each). Cells were stained with Hoechst 33258 dye, and nuclear morphology was revealed by fluorescent microscopy (described in Methods). Data shown are the mean ± SEM. *P < 0.05 versus untreated cells. (b) The ratio of apoptotic cells to total adherent cells in the dish after hypoxic injury. Cells were exposed to anoxia (12 hours) and percentage of nuclear fragmentation quantified under the following conditions: vehicle (control), DMSO (n = 4), white bars; wortmanin (n = 4), black bars; and PD98059 (n = 4), gray bars. Presence (8 U/ml) or absence of EPO is indicated by + and –, respectively. Cells were stained as above. *P < 0.05 versus vehicle-treated (DMSO), ^†P < 0.05 versus EPO alone. (c and d) Representative sample of H9c2 cells treated with H₂O₂ (200 μM) without EPO pretreatment (c) or with EPO (10 U/ml) for 24 hours (d). Arrows indicate fragmented nuclei under both conditions.