ArticleBMC genomics2010
Expression profiling of mouse embryonic fibroblasts with a deletion in the helicase domain of the Werner Syndrome gene homologue treated with hydrogen peroxide.
Article in BMC genomics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Epigallocatechin-3-gallate improves the quality of maternally aged oocytes.Cell proliferation · 2024Article
- Characterization of Stress Responses in aBiomolecules · 2021Article
- Chemical screen identifies a geroprotective role of quercetin in premature aging.Protein & cell · 2019Article
- Serum vitamin C levels modulate the lifespan and endoplasmic reticulum stress response pathways in mice synthesizing a nonfunctional mutant WRN protein.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Vitamin C alleviates aging defects in a stem cell model for Werner syndrome.Protein & cell · 2016Article
- Transient overexpression of Werner protein rescues starvation induced autophagy in Werner syndrome cells.Biochimica et biophysica acta · 2014Article
- Oxidative stress and antioxidant response in fibroblasts from Werner and atypical Werner syndromes.Aging · 2014Article
- Identification of RECQ1-regulated transcriptome uncovers a role of RECQ1 in regulation of cancer cell migration and invasion.Cell cycle (Georgetown, Tex.) · 2014Article
- Proteome-wide identification of WRN-interacting proteins in untreated and nuclease-treated samples.Journal of proteome research · 2011Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundWerner Syndrome (WS) is a rare disorder characterized by the premature onset of a number of age-related diseases. The gene responsible for WS encodes a DNA helicase/exonuclease protein believed to affect different aspects of transcription, replication, and/or DNA repair. In addition to genomic instability, human WS cells exhibit oxidative stress. In this report, we have examined the impact of exogenous hydrogen peroxide on the expression profile of mouse embryonic fibroblasts lacking part of the helicase domain of the WRN homologue (here referred to as Wrn Delta hel/Delta hel).
resultsWrn Delta hel/Delta hel mutant mouse embryonic fibroblasts exhibit increased oxidative stress. This was reflected by increased intracellular reactive oxygen species (ROS), increased oxidative damage in genomic DNA, changes in ATP/ADP ratios, and a disruption of the inner mitochondrial transmembrane potential when compared to wild type mouse embryonic fibroblasts. Expression profile analyses of hydrogen peroxide-treated wild type cells have indicated significant decreases in the expression of genes involved in mitosis, glycolysis, fatty acid metabolism, nucleic acid metabolism, and cell cycle control, as well as protein modification and stability. Such decreases in these biological processes were not observed in hydrogen peroxide-treated Wrn Delta hel/Delta hel cells. Importantly, untreated Wrn Delta hel/Delta hel cells already exhibited down regulation of several biological processes decreased in wild type cells that had been treated with hydrogen peroxide.
conclusionExpression profiling of Wrn Delta hel/Delta hel mutant cells revealed a very different response to exogenous addition of hydrogen peroxide in culture compared to wild type cells. This is due in part to the fact that Wrn Delta hel/Delta hel mutant cells already exhibited a modest chronic intracellular oxidative stress.
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