Figure 2.

Restoration of PINK1 rescues mitochondrial fragmentation, cell death, and neurite shortening in chronic MPP⁺-treated SH-SY5Y cells. Differentiated SH-SY5Y cells were treated with either vehicle (Veh) or 250 μm MPP⁺ for 2 weeks. There is a significant interaction between MPP⁺ treatment and PINK1 overexpression for all dependent variables analyzed (see Table 2). A–C, PINK1-GFP prevents mitochondrial fragmentation induced by chronic MPP⁺ treatment, as analyzed by mitochondrial elongation (*, p < 0.0001 for GFP (MPP⁺ versus vehicle); †, p < 0.0001 for MPP⁺ (PINK1-GFP versus GFP); B) and mitochondrial connectivity (*, p = 0.0007 for GFP (MPP⁺ versus vehicle); †, p = 0.0028 for MPP⁺ (PINK1-GFP versus GFP); C). D, PINK1-GFP rescues the decreased mitochondrial content (percentage of the area occupied by mitochondria per cell) caused by chronic MPP⁺ treatment. *, p = 0.0002 for GFP (MPP⁺ versus vehicle); †, p = 0.0003 for MPP⁺ (PINK1-GFP versus GFP). E, PINK1-GFP prevents chronic MPP⁺-induced cell death. *, p < 0.0001 for GFP (MPP⁺ versus vehicle); †, p = 0.0002 for MPP⁺ (PINK1-GFP versus GFP). F and G, PINK-GFP prevents chronic MPP⁺-induced neurite shortening. *. p = 0.001 for GFP (MPP⁺ versus vehicle); †. p = 0.0021 for MPP⁺ (PINK1-GFP versus GFP. All graphs represent means ± S.D.; n = 3 independent experiments for B–D and G; n = 4 independent experiments for E. The data were analyzed by two-way ANOVA with post hoc t tests (see Table 2 for analysis of main factors and interactions). Scale bars, 20 μm in A and 50 μm in F.