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. 2021 Feb 24;13:591475. doi: 10.3389/fnagi.2021.591475

Figure 7.

Figure 7

α-Syn treatment decreases the mitochondrial level of parkin in PC12 cells. (A) The immunoreactivity of parkin in mitochondrial (normalized relative to Ponceau-S) and cytosolic (normalized to GAPDH) extracts from pcDNA and pcDNA-Parkin PC12 cells treated with α-Syn for 24 h at a concentration of 5 μM. Data were log10 transformed and represent the mean value ± SD (mitochondria—n = 6, cytosol—n = 3) *p < 0.05, **p < 0.01, ***p < 0.001 compared to pcDNA control cells; ###p < 0.001 compared to pcDNA cells treated with α-Syn, using two-way ANOVA followed by Bonferroni post hoc test. (B) Representative photograph of Western blot analysis of ubiquitin and p62 in mitochondrial extracts from pcDNA and pcDNA-Parkin PC12 cells treated with α-Syn for 24 h at a concentration of 5 μM. (C) Immunoreactivity of ubiquitin normalized to Ponceau-S. Data were normalized to the untreated control group (=100%) and represent the mean value ± SD for six independent experiments (n = 6). **p < 0.01, ***p < 0.001 compared to pcDNA control cells; ###p < 0.001 compared to pcDNA cells treated with α-Syn, using two-way ANOVA followed by Bonferroni post hoc test. (D) Immunoreactivity of p62 normalized to Ponceau-S. Data were normalized to the untreated control group (= 100%) and represent the mean value ± SD for six independent experiments (n = 6). **p < 0.01 compared to pcDNA control cells; ###p < 0.001 compared to pcDNA cells treated with α-Syn, using two-way ANOVA followed by Bonferroni post hoc test.