Figure 1
From: Mitochondrial permeability transition pore induces mitochondria injury in Huntington disease
Effect of cell depolarization on calcium regulation in striatal cells. A, B striatal cells were loaded with Fluo3 AM and cytosolic calcium was measured using confocal microscopy. Fluo3 fluorescence changes were measured after cells were treated with 60 mM KCl for 30 min. Fluo3 intensity variations represent changes in cytosolic calcium levels and are expressed using the pseudo ratio ΔF/F0 (see Methods). B, quantitative analysis of 4 independent experiments of striatal cells treated with 60 mM KCl and 1 μM thapsigargin. No differences in cytosolic calcium peak were observed when wild type and mutant cells were compared. Data correspond to the mean ± S.E.M. of four independent experiments. * p < 0.05 compared with untreated wild type cells, ** p < 0.05 compared with untreated mutant cells, # p < 0.05 compared to with wild type cells treated with KCL, and ## p < 0.05 compared to mutant cells treated with KCL. C, D clonal striatal cells were loaded with Rhod2 AM/MitoGreen and treated with 60 mM KCl during 30 min for mitochondrial calcium determinations using confocal microscopy. KCl induced a mitochondrial calcium increase in both cell types, with no significant differences between wild type and mutant cells. Mitochondrial calcium levels were represented using pseudo ratio ΔF/F0. D, quantitative analysis of 4 independent experiments shows an increased mitochondrial calcium levels in both mutant and wild type cells exposed to KCl. Interestingly, mutant cells treated with 1 μM thapsigargin for 30 min showed a severe decrease in mitochondrial calcium uptake compared with wild type cells. Data correspond to the mean ± S.E.M. of four independent experiments. * p < 0.05 compared with wild type cells treated with KCl, ** p < 0.05 compared with mutant cells treated with KCl, and # p < 0.05 compared to mutant cells treated with KCL.