1. Fig. 7. Downstream effects of α-synuclein on mitochondria.
Downstream effects of α-synuclein on mitochondria. (A) In WT SH-SY5Y cells, a 24-hour exposure to oligomeric or dopamine-modified α-synuclein reduced basal and FCCP-stimulated mitochondrial respiration. Monomeric α-synuclein was without effect. *P < 0.01 versus vehicle, one-way ANOVA; n = 3. OCR, oxygen consumption rate. (B) In SH-SY5Y cells overexpressing TOM20, the deleterious effects of oligomeric and dopamine-modified α-synuclein were prevented. n = 3. (C) In WT HEK293 cells, a 24-hour exposure to oligomeric, dopamine-modified, or S129E α-synuclein induced oxidation of protein thiols, whereas exposure to monomeric or nitrated α-synuclein did not. (D and E) In HEK293 cells overexpressing TOM20, α-synuclein did not induce oxidative stress. At least 100 cells were quantified per condition in each experiment. aP < versus vehicle; bP < versus mock-transfected cells, two-way ANOVA; n = 3. (F) TMRM fluorescence in SH-SY5Y cells (as an index of ΔΨm) was reduced by oligomeric but not monomeric α-synuclein. (G and H) In SH-SY5Y cells overexpressing TOM20, oligomeric α-synuclein did not significantly affect ΔΨm. Thirty to 50 cells were analyzed for each treatment in each of three independent experiments. aP < versus vehicle; bP < versus WT cells, two-way ANOVA. Scale bars, 10 μm. Oligo, oligomycin; Rot, rotenone.
Roberto Di Maio et al., Sci Transl Med 2016;8:342ra78
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