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Fig. 2 | Molecular Neurodegeneration

Fig. 2

From: Mitovesicles secreted into the extracellular space of brains with mitochondrial dysfunction impair synaptic plasticity

Fig. 2

Murine Ts2 and human DS brain homogenates display similar protein alterations associated with mitochondrial fragmentation. (A-C) Representative Western blots (A) and densitometric quantifications (B, C) of proteins associated with mitochondrial fission in murine Ts2 brains (n = 3 males, 3 females) and human DS frontal cortices (n = 5 tissues from different human trisomic donors) as compared to their respective 2N controls (n = 3 male, 3 female diploid mice; n = 5 tissues from different human diploid donors). Two different pairs of mice for each sex are shown. DRP1 is master regulator of mitochondrial fragmentation (also known as fission) and is activated when phosphorylated at Ser616 (p-DRP1, upper band of the first row). MFF (mitochondrial fission factor) is an outer mitochondrial membrane integral protein and the recruiter of p-DRP1 to the mitochondrial surface. p-DRP1 levels were normalized to total DRP1, while MFF levels were normalized to β-actin. Sypro Ruby (total protein) staining was performed as a loading control. APP is one of the triplicated genes in both DS and in Ts2 mice and was used as an internal quality control to confirm the presence of the trisomy. Bars: mean ± SEM. Statistical tests used: two-tailed, unpaired Student’s t-test, with a different statistical test for each species, both in (B) and in (C). In (B): 2N vs. Ts2 (murine tissues) P = 0.0458; 2N vs. DS (human tissues) P = 0.0032. In (C): 2N vs. Ts2 (murine tissues) P = 0.0374; 2N vs. DS (human tissues) P = 0.0255. * P < 0.05, ** P < 0.01

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