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. 2015 Feb 2;9:16. doi: 10.3389/fncel.2015.00016

Figure 2.

Figure 2

Inactivation of p97 impairs mitochondrial function during neurotoxic stress. (A) SH-SY5Y cells stably expressing p97 or dominant-negative p97QQ under control of the Tet-On promoter were induced with tetracycline for 2 h or left uninduced and treated with 5 μM rotenone, 75 μM 6 OHDA, or 50 μM Aβ for an additional 6 h. Cells were stained with the mitochondrial membrane sensitive dye TMRE and analyzed by flow cytometry. (B) SH-SY5Y cells were treated with the p97 inhibitor DBeQ and mitochondrial membrane potential was measured by flow cytometric analysis of TMRE fluorescence. (C) Cells treated as in (A) were stained with the ROS-sensitive dye MitoSox and mitochondrial ROS generation was measured using flow cytometry. (D) SH-SY5Y cells were treated with the p97 inhibitor DBeQ and mitochondrial ROS generation was measured by flow cytometric analysis of MitoSox fluorescence. Statistical analysis was performed using pair-wise t-tests with Holm p-value adjustment for (A,C), and a general linear model (SPSS) for (B,D). Statistical significance is marked with n.s. for not significant, #p < 0.1, **p < 0.01, ***p < 0.001.