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Figure 2 | Molecular Neurodegeneration

Figure 2

From: Mitochondrial permeability transition pore induces mitochondria injury in Huntington disease

Figure 2

Treatment with Cyclosporine A prevents mitochondrial injury induced by thapsigargin in mutant HD cells. A, live confocal images of MitoRed, an indicator of mitochondrial potential, in striatal cells, untreated and treated with 1 μM thapsigargin (Th) for 30 min. Thapsigargin induces a significant decrease in the mitochondrial potential in mutant cells (see white arrows). Bar represents 10 μm. B, images show that CsA protects mutant huntingtin cells exposed to thapsigargin from mitochondrial impairment. Bar represents 10 μm. C, quantification of MitoRed intensities as relative units (ΔF/F0) in striatal cells treated for 30 min with experimental conditions as indicated. Data are the mean ± S.E.M. of 4 independent experiments. *, p < 0.05 compared with wild type cells treated with thapsigargin; ** p < 0.05 compared with mutant cells exposed to thapsigargin. D, correlation analysis of mitochondrial potential and cytosolic calcium observed in mutant cells treated with the indicated conditions for 30 min. Cytosolic calcium was estimated from the peak levels. Mitochondrial potential were obtained after 30 min of treatment for every condition. Data are expressed as the mean ± S.E.M. of 4 independent experiments. *, p < 0.05 compared to control; ** p < 0.05 compared to 60 mM KCL; ***, p < 0.05 compared to 4-BrA23187(1 nM) + 6 mM Ca2+. # compared to 60 mM KCL; ## compared to 4-BrA23187 + 6mM Ca2+. E, confocal images of mitochondrial potential in striatal cells, untreated and treated with 100 μM H2O2 for 1h. Bar represents 10 μm. F, striatal cells were incubated with 100 μM H2O2 for 1 h and mitochondrial potential was evaluated. MitoRed levels are show as relative units (ΔF/F0) at 1 h. Data is expressed as the mean ± S.E.M. of 3 independent experiments.

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