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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: Proteolytic cleavage of Beclin 1 exacerbates neurodegeneration

Fig. 7

C-Beclin 1 expression potentiates caspase 3 activation in neurons. a Timeline of primary hippocampal neuron experiments. Hippocampal neurons were isolated from E16.5 embryos. Neurons were infected at 1 week in vitro with lentivirues expressing Beclin 1 and a fluorescent reporter from a neuron-specific Synapsin promoter. Survival and cell death was assessed 2, 7 and 14 days post infection (P.I.). b Quantification of neuronal survival up to 14 days post infection. The number of GFP-positive, NeuN-positive neurons is expressed relative to the 2d control group (n = 10 wells/group/time point, 5 fields/well). Data expressed as mean + SEM. c Quantification of lactate dehydrogenase (LDH) released into the media from damaged cells as an additional measure of cell death and survival (n = 10 wells/group/time point). Data expressed as mean + SD. d Baseline caspase activation and neuronal cell loss was further quantified on the basis of caspase3/7 activity using a luminescent caspase-Glo substrate assay (n = 10 /group/time point). Data expressed as mean + SD. Overexpression of full-length (FL) Beclin 1 or its caspase cleavage products does not impact neuronal survival and caspase activation in the absence of any neurodegenerative insults. e Caspase activation was assessed using cleaved-caspase3 specific immunostaining in the hippocampus of mice expressing Beclin 1 isoforms in combination with Kainic acid or vehicle treatment (scale bar 75 μm). f Quantification of cleaved caspase 3 neurons in the CA1 region (n = 5–6 mice/group for the vehicle condition, n = 8–20 mice/group for the Kainic acid condition; 4–5 sections per mouse brain). C-beclin expression exacerbates caspase 3 activation in response to excitotoxic insults in vivo. *p < 0.05; one-way ANOVA with a Tukey’s post test for multiple comparisons

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