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. 2018 Apr 18;68(6):865–871. doi: 10.1007/s12576-018-0611-y

Fig. 3.

Fig. 3

MitoHK-II inactivation inhibits GSK3β-induced mPTP opening. a, b Time course of changes in calcein a and TMRE b intensities in GSK3β-treated permeabilized myocytes with and without glucose [glucose (–); ▽, glucose (+); ●]. Data are presented as the % of intensity at 0 min, and the values are mean ± SEM from 15 to 21 experiments. *P < 0.05 vs. GSK3β with glucose by two-way ANOVA followed with Bonferroni’s test. c Western-blot analysis of mitoHK-II after glucose-6-phosphate (G6P; 0, 0.01, 0.1, and 1 mmol/l) treatment in permeabilized myocytes. Data are presented as fold-increase of mitoHK-II/COXIV ratio from non-treated control (0 mmol/l), and the values are mean ± SEM from four independent experiments. *P < 0.05 vs. 0 mmol/l of G6P by one-way ANOVA with Kruskal–Wallis. d Time course of changes in mitochondrial calcein intensities. The permeabilized myocytes were perfused with GSK3β (●) or GSK3β plus G6P (▽, 0.01 mmol/l). Data are presented as the % of intensity at 0 min, and the values are mean ± SEM from 9 to 15 experiments. *P < 0.05 by two-way ANOVA followed with Bonferroni’s test