Skip to main content
. 2015 Nov 9;112(47):E6466–E6475. doi: 10.1073/pnas.1508760112

Fig. 2.

Fig. 2.

HAX-1 regulates the mitochondrial permeability transition pore. (A and B) Cyclosporine A abrogated the detrimental effect of HAX-1 heterozygous ablation on mitochondrial membrane potential after H2O2 treatment for 20 min. n = 4–8 hearts (>12 cells per heart); *P < 0.05 vs. WT with vehicle (DMSO) at 20 min; #P < 0.05 vs. HAX+/− with vehicle at 20 min. (C) Swelling induced by high calcium concentration in HAX-OE and WT mitochondria. n = 3 hearts for each group. (D) Inhibition of mitochondrial swelling required a lower cyclosporine A dose in HAX-1 overexpressing mitochondria. n = 3 hearts for each group. (E and F) Cyclosporine A abrogated the effect of HAX-1 on necrotic (E) and apoptotic (F) cell death. n = 8–15 hearts (>10,000 cells per heart); *P < 0.05 vs. WT at 2 mM H2O2; #P < 0.05 vs. the respective untreated group at 2 mM H2O2. Data are expressed as mean ± SEM.