Figure 7 | Cell Death & Differentiation

Figure 7

From: Mitochondrial dysfunction triggered by loss of HtrA2 results in the activation of a brain-specific transcriptional stress response

Figure 7

Antioxidants suppress neurodegeneration in HtrA2 KO mice. (a) Antioxidant treatment fails to suppress failure to gain weight in HtrA2 KO mice. Average body weight of control (HtrA2 WT and HET) and HtrA2 KO animals fed with either milk or milk supplemented with NAC. Mean values±S.E.M.; n=3. (b) Effect of antioxidants on the locomotor activity of male HtrA2 KO mice measured at P29. Data represented as scatter plot. (c) Features of localized striatal degeneration at P30 in control, HtrA2 KO mice and HtrA2 KO mice treated with NAC. Upper panels, NeuN staining, lower panels, immunofluorescence images showing GFAP staining (green) of astrocytes and Hoechst staining (purple) of cell nuclei. Scale bar corresponds to 400 μm. (d) NAC treatment of HtrA2 KO mice rescues neuronal loss. Density of NeuN-positive neurons in the area affected by HtrA2 loss at P30 in control, HtrA2 KO and HtrA2 KO mice treated with NAC. (e) NAC treatment of HtrA2 KO mice suppresses caspase-3 activation. Density of cells staining positive for cleaved caspase-3 in control, HtrA2 KO and HtrA2 KO mice treated with NAC. (f) Immortalized WT and HtrA2 KO MEFs were treated with vehicle, NAC (10 mM), 6-OHDA (25 μM) or a combination of both for 18 h. Transcript levels of CHOP are shown relative to vehicle control for same genotype. Data in (d, e, f) are represented as mean values±S.D.; n=3 in each group. Statistically significant values (one-way ANOVA with Bonferroni's post-test) relative to vehicle-treated WT are indicated for (b, d, e, f). *** for P<0.001, ** for P<0.01 and * for P<0.05

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