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Figure 4 | Skeletal Muscle

Figure 4

From: Protein phosphatase 2C-alpha knockdown reduces angiotensin II-mediated skeletal muscle wasting via restoration of mitochondrial recycling and function

Figure 4

PP2Cα knockdown did not restore AngII-mediated reductions in Akt or Fox0 phosphorylation or increased E3 ubiquitin ligase expression. All data were generated from experiments utilizing PP2Cα siRNA ‘A’. (A, B) Activating Akt phosphorylation was reduced with AngII, but not rescued by PP2Cα knockdown. (C) Akt-mediated inhibitory Fox0 phosphorylation was reduced with AngII, but not rescued by PP2Cα knockdown. (D) AMPK-mediated phosphorylation of FOXO3a was not altered by AngII or PP2Cα knockdown. (E) Expression of atrogin-1 mRNA was upregulated by AngII, but not rescued by PP2Cα knockdown. (F) Expression of MURF1 mRNA was upregulated by AngII, but not rescued by PP2Cα knockdown. (G) Expression of atrogin-1 protein was upregulated by AngII, but not rescued by PP2Cα knockdown. (H) No change in MURF1 protein expression was detected with AngII or PP2Cα siRNA. (I) Representative western blots showing effects of AngII and PP2Cα siRNA ‘A’ on the Akt-FOXO-E3 ligase signaling axis. n =6-20 per group, Mean ± SEM, *P <0.05, ***P <0.001 (Saline scrambled vs. AngII scrambled), +P <0.05 (AngII scrambled vs. AngII PP2Cα siRNA).

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Skeletal Muscle

ISSN: 2044-5040

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