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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mouse dermal fibroblasts exposed to hydrogen peroxide

ABSTRACT: Mouse dermal fibroblasts exposed to 0, 10 and 50mM of Hydrogen peroxide

ORGANISM(S): Mus musculus

SUBMITTER: George Garinis

PROVIDER: E-MEXP-1975 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity.

Garinis George A GA Uittenboogaard Lieneke M LM Stachelscheid Heike H Fousteri Maria M van Ijcken Wilfred W Breit Timo M TM van Steeg Harry H Mullenders Leon H F LH van der Horst Gijsbertus T J GT Brüning Jens C JC Niessen Carien M CM Hoeijmakers Jan H J JH Schumacher Björn B

Nature cell biology 20090412 5

The accumulation of stochastic DNA damage throughout an organism's lifespan is thought to contribute to ageing. Conversely, ageing seems to be phenotypically reproducible and regulated through genetic pathways such as the insulin-like growth factor-1 (IGF-1) and growth hormone (GH) receptors, which are central mediators of the somatic growth axis. Here we report that persistent DNA damage in primary cells from mice elicits changes in global gene expression similar to those occurring in various o ...[more]

PMID: 19363488

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2009-04-01 | E-MEXP-1968 | biostudies-arrayexpress

Transcription profiling of aorta from mice underexpressing Fibulin-4 to investigate its role in elastic fibre assembly and cardio-vasuclar disease

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Transcription profiling of liver from Csbm/m/Xpa-/- knockout mice to investigate the effect of nucleotide excision repair pathway inactivation

Project description:Cockayne syndrome (CS) is a photosensitive, DNA repair disorder associated with progeria caused by a defect in the transcription-coupled repair (TCR) subpathway of nucleotide excision repair (NER). Here, complete inactivation of NER in Csbm/m/Xpa-/- mutants causes a phenotype that reliably mimics the human progeroid CS syndrome. Newborn Csbm/m/Xpa-/- mice display attenuated growth, progressive neurological dysfunction, retinal degeneration, cachexia, kyphosis and die before weaning. To investigate whether a disturbance in growth and metabolism could explain the pronounced accelerated organismal deterioration seen in Csbm/m/Xpa-/- mice, we evaluated the liver transcriptome of 15-day old wt, single and double mutant mice (n=4). At this age, the Csbm/m/Xpa-/- pups have not yet become cachectic. Mouse liver transcriptome analysis and several physiological endpoints revealed systemic suppression of the GH/IGF1 somatotroph axis and oxidative metabolism, increased antioxidant responses, hypoglycemia together with hepatic glycogen and fat accumulation. Broad genome-wide parallels between Csbm/m/Xpa-/- and naturally aged mouse liver transcriptomes suggested that these changes are intrinsic to natural aging and the DNA repair-deficient mice. Importantly, wild type (wt) mice exposed to a low dose of chronic genotoxic stress and adult Csbm/m mutant mice recapitulated this response, thereby pointing to a novel link between genome instability and the age-related decline of the somatotroph axis.

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