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C/EBPβ regulates dexamethasone‐induced muscle cell atrophy and expression of atrogin‐1 and MuRF1
Author(s) -
Gonnella Patricia,
Alamdari Nima,
Tizio Steven,
Aversa Zaira,
Petkova Victoria,
Hasselgren PerOlof
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.23093
Subject(s) - myogenesis , muscle atrophy , myocyte , glucocorticoid , medicine , endocrinology , atrophy , chemistry , dexamethasone , protein degradation , downregulation and upregulation , biology , microbiology and biotechnology , skeletal muscle , biochemistry , gene
Muscle wasting in catabolic patients is in part mediated by glucocorticoids and is associated with increased expression and activity of the transcription factor C/EBPβ. It is not known, however, if C/EBPβ is causally linked to glucocorticoid‐induced muscle atrophy. We used dexamethasone‐treated L6 myoblasts and myotubes to test the role of C/EBPβ in glucocorticoid‐induced expression of the muscle‐specific ubiquitin ligases atrogin‐1 and MuRF1, protein degradation, and muscle atrophy by transfecting cells with C/EBPβ siRNA. In myoblasts, silencing C/EBPβ expression with siRNA inhibited dexamethasone‐induced increase in protein degradation, atrogin‐1 and MuRF1 expression, and muscle cell atrophy. Similar effects of C/EBPβ siRNA were seen in myotubes except that the dexamethasone‐induced increase in MuRF1 expression was not affected by C/EBPβ siRNA in myotubes. In additional experiments, overexpressing C/EBPβ did not influence atrogin‐1 or MuRF1 expression in myoblasts or myotubes. Taken together, our observations suggest that glucocorticoid‐induced muscle wasting is at least in part regulated by C/EBPβ. Increased C/EBPβ expression alone, however, is not sufficient to upregulate atrogin‐1 and MuRF1 expression. J. Cell. Biochem. 112: 1737–1748, 2011. © 2011 Wiley‐Liss, Inc.