miR-29b contributes to multiple types of muscle atrophy

Jin Li, Mun Chun Chan, Yan Yu, Yihua Bei, Ping Chen, Qiulian Zhou, Liming Cheng, Lei Chen, Olivia Ziegler, Glenn C. Rowe, Saumya Das and Junjie Xiao ()
Additional contact information
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
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

Nature Communications, 2017, vol. 8, issue 1, 1-15

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 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.

Date: 2017
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/ncomms15201 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15201

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms15201

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().