Oxidative Medicine and Cellular Longevity / 2018 / Article / Fig 3

Research Article

p66Shc Inactivation Modifies RNS Production, Regulates Sirt3 Activity, and Improves Mitochondrial Homeostasis, Delaying the Aging Process in Mouse Brain

Figure 3

Effects of aging on mitochondrial dynamics in p66Shc(−/−) mouse brain. Immunoblot of proteins separated using SDS-PAGE from purified brain mitochondria or whole brain lysate and RT-qPCR of mRNA from TRIzol-treated brain extracts were performed. The expression of the fusion proteins Mfn2 (a) and Opa1 (b), and the fission protein Drp1 (c) with its (S616) phosphorylated active isoform and mRNA levels of mouse brain in WT (grey) and p66Shc(−/−) (black) groups were observed at 3, 18, and 24 months of age. VDAC protein expression in mitochondrial fraction, actin protein expression in whole brain lysates, and GADPH mRNA levels in RT-qPCR were used as standard, respectively (, for each experimental group). Values represent the ; A represents compared to the 3-month-old group, B represents between 18- or 24-month-old WT and p66Shc(−/−) respective groups, one-way analysis of variance (ANOVA) and Bonferroni post hoc test.
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