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Angiotensin (1-7) Decreases Myostatin-Induced NF-κB Signaling and Skeletal Muscle Atrophy.

Authors
  • Aravena, Javier1, 2, 3
  • Abrigo, Johanna1, 2, 3
  • Gonzalez, Francisco1, 2, 3
  • Aguirre, Francisco1, 2, 3
  • Gonzalez, Andrea1, 2, 3
  • Simon, Felipe2, 4, 5
  • Cabello-Verrugio, Claudio1, 2, 3
  • 1 Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile. , (Chile)
  • 2 Millennium Institute on Immunology and Immunotherapy, 8370146 Santiago, Chile. , (Chile)
  • 3 Center for the Development of Nanoscience and Nanotechnology (CEDENNA), Universidad de Santiago de Chile, 8350709 Santiago, Chile. , (Chile)
  • 4 Millennium Nucleus of Ion Channels-Associated Diseases (MiNICAD), Universidad de Chile, 8370146 Santiago, Chile. , (Chile)
  • 5 Laboratory of Integrative Physiopathology, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, 8370146 Santiago, Chile. , (Chile)
Type
Published Article
Journal
International Journal of Molecular Sciences
Publisher
MDPI AG
Publication Date
Feb 10, 2020
Volume
21
Issue
3
Identifiers
DOI: 10.3390/ijms21031167
PMID: 32050585
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Myostatin is a myokine that regulates muscle function and mass, producing muscle atrophy. Myostatin induces the degradation of myofibrillar proteins, such as myosin heavy chain or troponin. The main pathway that mediates protein degradation during muscle atrophy is the ubiquitin proteasome system, by increasing the expression of atrogin-1 and MuRF-1. In addition, myostatin activates the NF-κB signaling pathway. Renin-angiotensin system (RAS) also regulates muscle mass. Angiotensin (1-7) (Ang-(1-7)) has anti-atrophic properties in skeletal muscle. In this paper, we evaluated the effect of Ang-(1-7) on muscle atrophy and signaling induced by myostatin. The results show that Ang-(1-7) prevented the decrease of the myotube diameter and myofibrillar protein levels induced by myostatin. Ang-(1-7) also abolished the increase of myostatin-induced reactive oxygen species production, atrogin-1, MuRF-1, and TNF-α gene expressions and NF-κB signaling activation. Ang-(1-7) inhibited the activity mediated by myostatin through Mas receptor, as is demonstrated by the loss of all Ang-(1-7)-induced effects when the Mas receptor antagonist A779 was used. Our results show that the effects of Ang-(1-7) on the myostatin-dependent muscle atrophy and signaling are blocked by MK-2206, an inhibitor of Akt/PKB. Together, these data indicate that Ang-(1-7) inhibited muscle atrophy and signaling induced by myostatin through a mechanism dependent on Mas receptor and Akt/PKB.

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