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. 2020 Feb 10;21(3):1167. doi: 10.3390/ijms21031167

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Prevention of myostatin-dependent muscle atrophy and signaling by Ang-(1-7) is mediated by the Akt/PKB activity in the myotubes. The C₂C₁₂ myotubes were incubated with myostatin (Mstn, 1 µg/mL) for 12 or 24 h in the presence or absence of Ang-(1-7) (10 nM), MK2206 (10 µM; pre-incubated for 30 min), or both. The parameters measured were as follows: (A) distribution of the myotube diameters; mRNA levels of (B) atrogin-1, (C) MuRF-1 and (E) TNF-α; (D) Luciferase activity of pNF-κB-luc; and (F) ROS levels. The values are expressed as a fold of induction relative to the myotubes without treatment, and correspond to the mean ± SD from three independent experiments (n = 3; * p < 0.05 vs. control without treatment).

Prevention of myostatin-dependent muscle atrophy and signaling by Ang-(1-7) is mediated by the Akt/PKB activity in the myotubes. The C₂C₁₂ myotubes were incubated with myostatin (Mstn, 1 µg/mL) for 12 or 24 h in the presence or absence of Ang-(1-7) (10 nM), MK2206 (10 µM; pre-incubated for 30 min), or both. The parameters measured were as follows: (A) distribution of the myotube diameters; mRNA levels of (B) atrogin-1, (C) MuRF-1 and (E) TNF-α; (D) Luciferase activity of pNF-κB-luc; and (F) ROS levels. The values are expressed as a fold of induction relative to the myotubes without treatment, and correspond to the mean ± SD from three independent experiments (n = 3; * p < 0.05 vs. control without treatment).