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TGF-β requires the activation of canonical and non-canonical signalling pathways to induce skeletal muscle atrophy by Johanna Ábrigo; Fabian Campos; Felipe Simon; Claudia Riedel; Daniel Cabrera; Cristian Vilos; Claudio Cabello-Verrugio is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.

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## Abstract The transforming growth factor type-beta (TGF-β) induces skeletal muscle atrophy characterised by a decrease in the fibre’s diameter and levels of myosin heavy chain (MHC), also as an increase of MuRF-1 expression. In addition, TGF-β induces muscle atrophy by a mechanism dependent on reactive oxygen species (ROS). TGF-β signals by activating both canonical Smad-dependent, and non-canonical signalling pathways such as ERK1/2, JNK1/2, and p38 MAPKs. However, the participation of canonical and non-canonical signalling pathways in the TGF-β atrophic effect on skeletal muscle is unknown. We evaluate the impact of Smad and MAPK signalling pathways on the TGF-β-induced atrophic effect in C~2~C~12~ myotubes. The results indicate that TGF-β activates Smad2/3, ERK1/2 and JNK1/2, but not p38 in myotubes. The pharmacological inhibition of Smad3, ERK1/2 and JNK1/2 activation completely abolished the atrophic effect of TGF-β. Finally, the inhibition of these canonical and non-canonical pathways did not decrease the ROS increment, while the inhibition of ROS production entirely abolished the phosphorylation of Smad3, ERK1/2 and JNK1/2. These results suggest that TGF-β requires Smad3,

Who reads TGF-β requires the activation of canonical and non-canonical signalling pathways to induce skeletal muscle atrophy?

Author

Johanna Ábrigo; Fabian Campos; Felipe Simon; Claudia Riedel; Daniel Cabrera; Cristian Vilos; Claudio Cabello-Verrugio

Publisher

Walter de Gruyter GmbH

Published

2017

Language

EN

Field

Biochemistry, Genetics and Molecular Biology (Life Sciences)