File(s) under permanent embargo
NDRG2, a novel regulator of myoblast proliferation, is regulated by anabolic and catabolic factors
journal contribution
posted on 2009-04-01, 00:00 authored by Victoria Foletta, Matthew Prior, Nicole Stupka, K Carey, D Segal, Sharon Jones, Courtney SwintonCourtney Swinton, Sheree Martin, David Cameron-Smith, Ken WalderKen WalderSkeletal muscle tissue undergoes adaptive changes in response to stress and the genes that control these processes are incompletely characterised. NDRG2 (N-myc downstream-regulated gene 2), a stress- and growth-related gene, was investigated in skeletal muscle growth and adaption. While NDRG2 expression levels were found to be up-regulated in both differentiated human and mouse myotubes compared with undifferentiated myoblasts, the suppression of NDRG2 in C2C12 myoblasts resulted in slowed myoblast proliferation. The increased expression levels of the cell cycle inhibitors, p21 Waf1/Cip1 and p27 Kip1, and of various muscle differentiation markers in NDRG2-deficient myoblasts indicate that a lack of NDRG2 promoted cell cycle exiting and the onset of myogenesis. Furthermore, the analysis of NDRG2 regulation in C2C12 myotubes treated with catabolic and anabolic agents and in skeletal muscle from human subjects following resistance exercise training revealed NDRG2 gene expression to be down-regulated during hypertrophic conditions, and conversely, up-regulated during muscle atrophy. Together, these data demonstrate that NDRG2 expression is highly responsive to different stress conditions in skeletal muscle and suggest that the level of NDRG2 expression may be critical to myoblast growth and differentiation.
History
Journal
Journal of physiologyVolume
587Issue
7Pagination
1619 - 1634Publisher
Wiley-BlackwellLocation
Oxford, EnglandPublisher DOI
ISSN
0022-3751eISSN
1469-7793Language
engPublication classification
C1 Refereed article in a scholarly journalCopyright notice
2009, The Authors.Usage metrics
Categories
No categories selectedKeywords
Licence
Exports
RefWorks
BibTeX
Ref. manager
Endnote
DataCite
NLM
DC