Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Microarray analysis of skeletal muscle hypertrophy induced by heat-stress in healthy humans

ABSTRACT: This study was aimed at examining the effects of long-term of heat-stress on the gene expression of skeletal muscle hypertrophy. Heat- and stream-generating (HSG) sheets were placed on thigh laterally. The HSG sheets (heat-stress) were applied 8-hrs/day, once a day, 4 days/weeks, for 10 weeks. A muscle biopsy was taken from the vastus lateralis muscle (2 cm depth) of the treated leg before and after the experiment. Oligonucleotide microarray revealed that genes related to ATP-synthesis, protein synthesis and the molecular chaperonic activity were increased by heat stress. These results suggest that heat-stress might be a useful countermeasure for muscular atrophy during aging. Overall design: Five subjects were applied by heat- and stream-generating (HSG) sheets for 10 weeks. Total RNAs obtained from the skeletal muscle before and after the experiment were used for the analysis.

ORGANISM(S): Homo sapiens

SUBMITTER: Hidehiko Kondo

PROVIDER: E-GEOD-12474 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Recent studies on mouse and human skeletal muscle (SM) demonstrated the important link between mitochondrial function and the cellular metabolic adaptation. To identify key compensatory molecular mechanisms in response to chronic mitochondrial distress, we analyzed mice with ectopic SM respiratory uncoupling in uncoupling protein 1 transgenic (UCP1-TG) mice as model of muscle-specific compromised mitochondrial function. Here we describe a detailed metabolic reprogramming profile associated with mitochondrial perturbations in SM, triggering an increased protein turnover and amino acid metabolism with induced biosynthetic serine/1-carbon/glycine pathway and the longevity-promoting polyamine spermidine as well as the trans-sulfuration pathway. This is related to an induction of NADPH-generating pathways and glutathione metabolism as an adaptive mitohormetic response and defense against increased oxidative stress. Strikingly, consistent muscle retrograde signaling profiles were observed in acute stress states such as muscle cell starvation and lipid overload, muscle regeneration, and heart muscle inflammation, but not in response to exercise. We provide conclusive evidence for a key compensatory stress-signaling network that preserves cellular function, oxidative stress tolerance, and survival during conditions of increased SM mitochondrial distress, a metabolic reprogramming profile so far only demonstrated for cancer cells and heart muscle.-Ost, M., Keipert, S., van Schothorst, E. M., Donner, V., van der Stelt, I., Kipp, A. P., Petzke, K.-J., Jove, M., Pamplona, R., Portero-Otin, M., Keijer, J., and Klaus, S. Muscle mitohormesis promotes cellular survival via serine/glycine pathway flux. Control C57BL/6J wildtype male mice, aged 12 weeks, are compared to UCP1 transgene littermates fed purified low fat diet (BIOCLAIMS, Hoevenaars et al., Genes and Nutrition 2012) for 12 weeks . At the end, mice were sacrificed, gastrocnemius skeletal muscle was immediately dissected and snap frozen in liquid nitrogen. Total RNA was isolated, quantified and qualified, and subsequently used for global gene expression profiling using Agilent 8x60K microarrays. In total, 6 arrays of individual WT and 7 arrays of individual UCP1-TG samples were normalized, together with samples from the complete SUPERSERIES.

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Microarray analysis of skeletal muscle hypertrophy induced by heat-stress in healthy humans

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