Angiotensin-(1-7) Prevents Skeletal Muscle Atrophy Induced by Transforming Growth Factor Type Beta (TGF-β) via Mas Receptor Activation
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Archivos
Fecha
2016
Profesor/a Guía
Facultad/escuela
Idioma
en
Título de la revista
ISSN de la revista
Título del volumen
Editor
KARGER
Nombre de Curso
Licencia CC
Licencia CC
Resumen
Background: Transforming growth factor type beta 1 (TGF-131) produces skeletal muscle atrophy. Angiotensin-(1-7) (Ang-(1-7)), through the Mas receptor, prevents the skeletal muscle atrophy induced by sepsis, immobilization, or angiotensin II (Ang-II). However, the effect of Ang(1-7) on muscle wasting induced by TGF-beta 1 is unknown. Aim: To evaluate whether Ang-(1-7)/Mas receptor axis could prevent the skeletal muscle atrophy induced by TGF-131. Methods: This study assessed the atrophic effect of TGF-beta 1 in C2C12, myotubes and mice in absence or presence of Ang-(1-7), and the receptor participation using A779, an antagonist of the Mas receptor. The levels of myosin heavy chain (MHC), polyubiquitination, and MuRF-1 were detected by western blot. Myotube diameter was also evaluated. In vivo analysis included the muscle strength, fibre diameter, MHC and MuRF-1 levels by western blot, and ROS levels by DCF probe detection. Results: The results showed that Ang-(1-7) prevented the increase in MuRF-1 and polyubiquitined protein levels, the decrease of MHC levels, the myotubes/ fibre diameter diminution, and the increased production of reactive oxygen species (ROS) induced by TGF-beta 1. Utilizing A779 inhibited the anti-atrophic effect of Ang-(1-7). Conclusion: The preventive effect of Ang-(1-7) on skeletal muscle atrophy induced by TGF-beta 1 is produced through inhibition of ROS production and proteasomal degradation of MHC. (C) 2016 The Author(s) Published by S Karger AG, Basel
Notas
Indexación: Web of Science; Scielo.
Palabras clave
Muscle wasting, TGF-beta, ng-(1-7), Mas receptor, MHC, MuRF-1
Citación
Cell Physiol Biochem 2016;40:27-38