Fig. 6: TOM40 supplementation partially mitigates α-Syn-induced mitochondrial defects. | Cell Death & Disease

Fig. 6: TOM40 supplementation partially mitigates α-Syn-induced mitochondrial defects.

From: Mitochondria-targeted oligomeric α-synuclein induces TOM40 degradation and mitochondrial dysfunction in Parkinson’s disease and parkinsonism-dementia of Guam

Fig. 6

A Assessment of cell viability with MTT assay after 48 h of induced α-Syn overexpression. B Measurement of mitochondrial membrane potential with TMRE assay results following 48 h of induced α-Syn overexpression. C Representative epifluorescence/phase-contrast image of WT α-Syn cells infected with TOM40 eGFP Lv-C-Flag-SV40-eGFP infection, scale bar = 20 µm. D, E Representative immunoblot and densitometry analysis demonstrating TOM40 overexpression level post-infection. F Seahorse analysis presenting an overview of Oxygen Consumption Rate (OCR) in WT α-Syn Dox (-), Dox (+), and Dox (+) plus TOM40 overexpression (TOM40 OE) cells during the mitochondrial respiration test. G Basal respiration in WT α-Syn overexpressing cells. H ATP-linked respiration. I Maximal respiration was assessed following mitochondrial uncoupling by FCCP. J Spare respiratory capacity is determined by subtracting basal respiration from maximal respiration in WT α-Syn overexpressing cells. K Proton leakage was evaluated after inhibiting complex III via antimycin-A. L Non-mitochondrial oxygen consumption. Data (A, B, E) are presented as mean ± s.e.m. from three independent experiments, and data (F–L) are presented as presented mean ± s.e.m. from four independent experiments. The statistical analyses were performed using two-way ANOVA (A, B) and one-way ANOVA (E–L). non-significant (p > 0.05).

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