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: Article

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

Huella dactilar

Muscular Atrophy
Angiotensins
Angiotensin II
Muscle
Skeletal Muscle
Apoptosis
Recovery
Muscle Strength
Renin-Angiotensin System
Ubiquitin
Diaphragm
Muscles
Diaphragms
Renin
Peptides
Caspase 9
Caspase 8
Proteasome Endopeptidase Complex
Ligases
Caspase 3

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

Citar esto

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title = "The angiotensin-(1–7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice",
abstract = "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.",
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The angiotensin-(1–7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice. / Meneses, Carla; Morales, María Gabriela; Abrigo, Johanna; Simon, Felipe; Brandan, Enrique; Cabello-Verrugio, Claudio.

En: Pflugers Archiv European Journal of Physiology, Vol. 467, N.º 9, A001, 01.09.2015, p. 1975-1984.

Resultado de la investigación: Article

TY - JOUR

T1 - The angiotensin-(1–7)/Mas axis reduces myonuclear apoptosis during recovery from angiotensin II-induced skeletal muscle atrophy in mice

AU - Meneses, Carla

AU - Morales, María Gabriela

AU - Abrigo, Johanna

AU - Simon, Felipe

AU - Brandan, Enrique

AU - Cabello-Verrugio, Claudio

PY - 2015/9/1

Y1 - 2015/9/1

N2 - 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.

AB - 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.

KW - Angiotensin

KW - Apoptosis

KW - Muscle wasting

KW - Proteasome

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U2 - 10.1007/s00424-014-1617-9

DO - 10.1007/s00424-014-1617-9

M3 - Article

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AN - SCOPUS:84943362741

VL - 467

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EP - 1984

JO - Pflugers Archiv European Journal of Physiology

JF - Pflugers Archiv European Journal of Physiology

SN - 0031-6768

IS - 9

M1 - A001

ER -