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. 2012 Feb 2;8(2):e1002488. doi: 10.1371/journal.pgen.1002488

Figure 4. Alterations in TRAP1 levels influence [A53T]α-Synuclein-induced sensitivity to oxidative stress and mitochondrial effects in HEK293 cells.

Figure 4

HEK293 cells were transfected with plasmids promoting [A53T]α-Synuclein or TRAP1 expression. Empty vector transfection served as control. In addition, RNAi-mediated silencing of endogenous TRAP1 was induced (siTRAP1). Cells transfected with indicated plasmid combinations were treated with (A) hydrogen peroxide (100 µm) or (B) rotenone (200 µM) to induce oxidative stress. Cell numbers were analyzed to monitor survival. (C–E) HEK293 without oxidative stress treatment overexpressing the indicated proteins, or with RNAi-mediated silencing of TRAP1 were analyzed for (C) ATP production via Complex I, (D) total ATP content, and (E) mitochondrial membrane potential. Statistical analysis of displayed bar graphs was performed using ANOVA followed by Newman-Keuls Multiple Comparison Test. (A, B) Biologically relevant comparisons are indicated in bar graphs. (C) Differences compared to control are indicated. (A, B, C) A detailed summary of all comparisons is summarized in Figure S8. (D, E) Only cells with [A53T]α-Synuclein expression and TRAP1 reduction displayed significant differences in statistical analysis as indicated in graph. All other comparisons were not significant. *p<0.05; **p<0.01; ***p<0.001; ns = not significant.