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Transcriptional effects of forced KLF15 over-expression in mouse muscle.

ABSTRACT: Excessive or sustained glucocorticoid (GC) exposure causes muscle wasting. Paradoxically, moderate or transient GC exposure elicits ergogenic effects, evidenced by their widespread use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle wasting disease. While mechanisms underlying GC-mediated muscle wasting are well defined, the molecular basis for the latter remains unknown. In this arm of our studies, we compare expression profiles in quadriceps tissue from KLF15 transgenic (MTg) and non-Tg mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE74623 | GEO | 2015/12/01

SECONDARY ACCESSION(S): PRJNA301033

REPOSITORIES: GEO

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KLF15- and glucocorticoid-dependent transcriptional responses in mouse muscle.

Project description:Excessive or sustained glucocorticoid (GC) exposure causes muscle wasting. Paradoxically, moderate or transient GC exposure elicits ergogenic effects, evidenced by their widespread use as doping agents by endurance athletes and poorly understood efficacy in Duchenne muscular dystrophy (DMD), a genetic muscle wasting disease. While mechanisms underlying GC-mediated muscle wasting are well defined, the molecular basis for the latter remains unknown. In this arm of our studies, Wild-type (WT) and Klf15-/- (KO) mice were given the potent GC receptor agonist dexamethasone (dex) and quadriceps tissue was subjected to transcript expression profiling by cDNA microarrays.

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