Skip to main content
. 2015 Dec 4;310(3):H376–H384. doi: 10.1152/ajpheart.00748.2015

Fig. 4.

Fig. 4.

MDL treatment inhibited mitochondrial permeability transition pore (MPTP) opening in mouse heart mitochondria following IR. CRC (calcium retention capacity) was used to measure MPTP opening in mouse heart mitochondria following IR. A: a representative original tracing in each group is shown. B: IR markedly decreased the CRC compared with TC, whereas MDL treatment improved the CRC compared with untreated. These results support that activation of calpains contributes to MPTP opening during IR. Values are means ± SE; n = 5–7 in each group. *P < 0.05 vs. TC. †P < 0.05 vs. untreated hearts. Inner mitochondria membrane potential (Δψ) was used to reflect MPTP opening in mitochondria already incubated with exogenous calcium. C: the original tracing in each group is shown. D: exogenous calcium dose-dependently depolarized the Δψ in mouse heart mitochondria. Cyclophilin A prevented the calcium-induced depolarization of the Δψ, supporting that the depolarization of the Δψ was due to MPTP opening. MDL treatment decreased the extent of the Δψ depolarization compared with untreated mitochondria, suggesting that activation of mit-CPN1 sensitizes to MPTP opening. Values are means ± SE; n = 4 in each group. *P < 0.05 vs. noncalcium-treated mitochondria. †P < 0.05 vs. non-MDL-treated mitochondria. ‡P < 0.05 vs. calcium-treated mitochondria in the presence or absence of MDL. TMRM, tetramethylrhodamine methyl ester; AU, arbitrary units.