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MiR-29b contributes to multiple types of muscle atrophy.


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-? and H2O2 treatment. Targeting of IGF-1 and PI3K(p85?) 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(p85?), and that suppression of miR-29b may represent a therapeutic approach for muscle atrophy induced by different stimuli.

SUBMITTER: Li J 

PROVIDER: S-EPMC5458521 | biostudies-literature | 2017 May

REPOSITORIES: biostudies-literature

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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<sub>2</sub>O<sub>2</sub> treatment. Targeting of  ...[more]

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