Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide analysis of dexamethasone-responsive gene expression in mouse triceps surae muscle

ABSTRACT: Analysis of dexamethasone-regulation of muscle mass at gene expression level. The hypothesis tested in the present study was that the presence of MuRF1 contributes to the extent of gene expression changes observed in specific sets of genes during a challenge leading to muscle atrophy. Results provide important information on the response of triceps surae muscle to synthetic glucocorticoid treatment, such as specific cell signaling and metabolic enzyme genes, that may be influenced by MuRF1 during atrophy. Total RNA obtained from isolated triceps surae muscle subjected to 3 or 14 days dexamethasone treatment compated to untreated littermate control muscles.

ORGANISM(S): Mus musculus

SUBMITTER: J. Furlow

PROVIDER: E-GEOD-44208 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Glucocorticoids are a well recognized and common cause of muscle atrophy. Glucocorticoid-induced atrophy can be prevented by testosterone, but the molecular mechanisms underlying such protection have not been described. Thus, the global effects of testosterone on dexamethasone-induced changes in gene expression were evaluated in rat gastrocnemius muscle using Affymetrix 230_2 DNA microarrays. Gene expression was analyzed after 7 days administration of dexamethasone, dexamethasone plus testosterone, or vehicle. Effects of these agents on weights of gastrocnemius muscles from these animals has been reported (1. Zhao W, Pan J, Zhao Z, Wu Y, Bauman WA, and Cardozo CP. Testosterone protects against dexamethasone-induced muscle atrophy, protein degradation and MAFbx upregulation. J Steroid Biochem Mol Biol 110: 125-129, 2008.) Dexamethasone changed expression of 876 probe sets by at least 2-fold, of which 474 probe sets were changed by at least two fold in the opposite direction in the dexamethasone plus testosterone group (genes in opposition). Major biological themes represented by genes in opposition included IGF-1 signaling, protein synthesis, myogenesis and muscle development, and ubiquitin conjugases and ligases. Testosterone blocked increased expression of DDIT4 and eIF4EBP1, FOXO1 and of the p85 regulatory subunit of the IGF-1 receptor, while preventing decreased expression of IRS-1. Testosterone blocked decreased expression of LXR and suppressed upregulation of C/EBP beta and delta. Testosterone prevented increase expression of Cdkn1A (p21) and decrease expression of cyclins B and D, as well as many other changes that would be expected to reduce cell cycle progression. Testosterone prevented increased expression of muscle development factors Csrp3 and Mbn1 and blocked reduced expression of Wnt4. These data suggest that testosterone blocks multiple changes in gene expression that, collectively, would otherwise downregulate molecular signals that promote protein synthesis and muscle hypertrophy and that stimulate muscle protein catabolism. Experiment Overall Design: Rats (250 g males) were administered dexamethasone (0.7 mg/kg/day) alone or with testosterone (20 mg/kg/day) dissolved in vehicle (propylene glycol) by continuous infusion (Alzet pumps) for 7 days. Control animals were administered vehicle only. Gene expression was compared among the 3 groups at 7 days using one chip per animal, 3 animals per group.

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Genome-wide analysis of dexamethasone-responsive gene expression in mouse triceps surae muscle

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