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- W3020820276 abstract "Circulating Angiotensin II (AngII) is elevated in congestive heart failure (CHF), and leads to skeletal muscle wasting, which is strongly associated with poor patient outcomes. We previously found that AngII upregulates protein phosphatase 2C-alpha (PP2Cα) and dephosphorylates AMP-Activated Protein Kinase (AMPK), a critical regulator of cellular metabolism, in skeletal muscle. To determine the role of PP2Cα in AngII-induced wasting, gastrocnemius (Gas) muscles of FVB mice were injected with scrambled or PP2Cα siRNA and mice were infused with saline or AngII for 4 days. Knockdown of PP2Cα reduced AngII wasting by 50% (p<0.001), blocked AngII upregulation of PP2Cα by 62% (p<0.01), increased p-T172-AMPK by 60% versus scrambled siRNA (p<0.01), and inhibited AngII-mediated reductions in peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α, p<0.05), in complex IV activity (p<0.01), and in ATP (p<0.05) by 35-51%. AngII impaired autophagic flux as determined by a 165% increase in p62/SQSTM1 (p62) e..." @default.
- W3020820276 created "2020-05-13" @default.
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- W3020820276 date "2014-11-25" @default.
- W3020820276 modified "2023-09-26" @default.
- W3020820276 title "Abstract 13912: Protein Phosphatase 2C-alpha Knockdown Reduces Angiotensin II-Mediated Skeletal Muscle Wasting via Restoration of Mitochondrial Recycling and Function" @default.
- W3020820276 hasPublicationYear "2014" @default.
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