The angiotensin-(1–7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice

Carla Meneses, María Gabriela Morales, Johanna Abrigo, Felipe Simon, Enrique Brandan, Claudio Cabello-Verrugio

Resultado de la investigación: Contribución a una revistaArtículo

33 Citas (Scopus)

Resumen

Angiotensin-(1–7) [Ang (1–7)] is a peptide belonging to the non-classical renin-angiotensin system (RAS). Ang (1–7), through its receptor Mas, has an opposite action to angiotensin II (Ang II), the typical peptide of the classical RAS axis. Ang II produces skeletal muscle atrophy, a pathological condition characterised by the loss of strength and muscle mass. A feature of muscle atrophy is the decrease of the myofibrillar proteins produced by the activation of the ubiquitin-proteasome pathway (UPP), evidenced by the increase in the expression of two muscle-specific ubiquitin ligases: atrogin-1 and MuRF-1. In addition, it has been described that Ang II also induces myonuclear apoptosis during muscle atrophy.We assessed the effects of Ang (1–7) and Mas participation on myonuclear apoptosis during skeletal muscle atrophy induced by Ang II. Our results show that Ang (1–7), through Mas, prevents the effects induced by Ang II in the diaphragm muscles and decreases several events associated with apoptosis in the diaphragm (increased apoptotic nuclei, increased expression of caspase-8 and caspase-9, increased caspase-3 activity and increased Bax/Bcl-2 ratio). Concomitantly, Ang (1–7) also attenuates the decrease in fibre diameter and muscle strength, and prevents the increase in atrogin-1 and MuRF-1 during the muscle wasting induced by Ang II. Interestingly, these effects of Ang (1–7) are dependent on the Mas receptor. Thus, we demonstrated for the first time that Ang (1–7) prevents myonuclear apoptosis during the recovery of skeletal muscle atrophy induced by Ang II.

Idioma originalInglés
Número de artículoA001
Páginas (desde-hasta)1975-1984
Número de páginas10
PublicaciónPflugers Archiv European Journal of Physiology
Volumen467
N.º9
DOI
EstadoPublicada - 1 sep 2015

Áreas temáticas de ASJC Scopus

  • Fisiología
  • Bioquímica clínica
  • Fisiología (médica)

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