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NDRG2, a novel regulator of myoblast proliferation, is regulated by anabolic and catabolic factors
Author(s) -
Foletta Victoria C.,
Prior Matthew J.,
Stupka Nicole,
Carey Kate,
Segal David H.,
Jones Sharon,
Swinton Courtney,
Martin Sheree,
CameronSmith David,
Walder Ken R.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2008.167882
Subject(s) - myogenesis , c2c12 , myocyte , skeletal muscle , anabolism , microbiology and biotechnology , biology , muscle atrophy , cell growth , myogenin , gene expression , endocrinology , chemistry , gene , genetics
Skeletal 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.