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miR-29b contributes to multiple types of muscle atrophy

Author

Listed:
  • Jin Li

    (Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University)

  • Mun Chun Chan

    (Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School
    Georgetown University)

  • Yan Yu

    (Tongji Hospital, Tongji University School of Medicine)

  • Yihua Bei

    (Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University)

  • Ping Chen

    (Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University)

  • Qiulian Zhou

    (Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University)

  • Liming Cheng

    (Tongji Hospital, Tongji University School of Medicine)

  • Lei Chen

    (Tongji Hospital, Tongji University School of Medicine)

  • Olivia Ziegler

    (Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School)

  • Glenn C. Rowe

    (The University of Alabama at Birmingham)

  • Saumya Das

    (Cardiovascular Division of the Massachusetts General Hospital and Harvard Medical School)

  • Junjie Xiao

    (Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University)

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 H2O2 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.

Suggested Citation

  • Jin Li & Mun Chun Chan & Yan Yu & Yihua Bei & Ping Chen & Qiulian Zhou & Liming Cheng & Lei Chen & Olivia Ziegler & Glenn C. Rowe & Saumya Das & Junjie Xiao, 2017. "miR-29b contributes to multiple types of muscle atrophy," Nature Communications, Nature, vol. 8(1), pages 1-15, August.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15201
    DOI: 10.1038/ncomms15201
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    Cited by:

    1. Sneha Mishra & Claudia Cosentino & Ankit Kumar Tamta & Danish Khan & Shalini Srinivasan & Venkatraman Ravi & Elena Abbotto & Bangalore Prabhashankar Arathi & Shweta Kumar & Aditi Jain & Anand S. Ramai, 2022. "Sirtuin 6 inhibition protects against glucocorticoid-induced skeletal muscle atrophy by regulating IGF/PI3K/AKT signaling," Nature Communications, Nature, vol. 13(1), pages 1-22, December.

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