miR-29b contributes to multiple types of muscle atrophy

Jin Li(Shanghai University), Mun Chun Chan(Harvard University), Yan Yu(Tongji University), Yihua Bei(Shanghai University), Ping Chen(Shanghai University), Qiulian Zhou(Shanghai University), Liming Cheng(Tongji University), Lei Chen(Tongji University), Olivia Ziegler(Harvard University), Glenn C. Rowe(University of Alabama at Birmingham), Saumya Das(Harvard University), Junjie Xiao(Shanghai University)
Nature Communications
May 25, 2017
Cited by 245Open Access
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Abstract

Abstract A number of microRNAs (miRNAs, miRs) have been shown to play a role in skeletal muscle atrophy, but their role is not completely understood. Here we show that miR-29b promotes skeletal muscle atrophy in response to different atrophic stimuli in cells and in mouse models. miR-29b promotes atrophy of myotubes differentiated from C2C12 or primary myoblasts, and conversely, its inhibition attenuates atrophy induced by dexamethasone (Dex), TNF-α and H 2 O 2 treatment. Targeting of IGF-1 and PI3K(p85α) by miR-29b is required for induction of muscle atrophy. In vivo , miR-29b overexpression is sufficient to promote muscle atrophy while inhibition of miR-29b attenuates atrophy induced by denervation and immobilization. These data suggest that miR-29b contributes to multiple types of muscle atrophy via targeting of IGF-1 and PI3K(p85α), and that suppression of miR-29b may represent a therapeutic approach for muscle atrophy induced by different stimuli.


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