Fig. 2: MGO-treatment induces the accumulation of aSyn and AGEs in the midbrain.
From: Glycation modulates glutamatergic signaling and exacerbates Parkinson’s disease-like phenotypes
Wild-type littermate (WT) and Thy1-aSyn transgenic mice received an intracerebroventricular (ICV) injection of MGO or vehicle (PBS) and protein brain extracts from several regions analyzed 5 weeks post injection. Protein extracts were resolved by SDS-PAGE or loaded into membranes in a dot-blot system (see Supplementary Fig. 2). Membranes were probed with anti-aSyn, anti-CEL, anti-pS129-aSyn and anti-β-actin for normalization. Representative blots showing two samples from each experimental group are shown for aSyn, and densitometric analysis represented for aSyn and CEL in a, b midbrain, c, d striatum, e, f cerebellum, g, h prefrontal cortex, and i, j hippocampus, respectively. k Representative blot showing four samples from vehicle- and MGO-injected Thy1-aSyn mice are shown for pS129-aSyn and aSyn total signal. Densitometric analysis of the ratio between pS129-aSyn and aSyn is presented. l Representative blot showing aSyn probing in soluble and insoluble fraction from vehicle- and MGO-injected Thy1-aSyn mice. Densitometric analysis of the ratio between the insoluble and the sum of both soluble and insoluble signals is presented. At least n = 5 in all groups, data in all panels are average with error bars representing standard deviation, Ordinary one-way ANOVA, *p < 0.05, **p < 0.01, ****p < 0.0001; unpaired two-tailed t-test with equal SD, #p < 0.05.
