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• W2091658446 abstract "Werner syndrome (WS) is a rare autosomal disease characterized by the premature onset of several age-associated pathologies. The protein defective in WS patients (WRN) is a helicase/exonuclease involved in DNA repair, replication, transcription and telomere maintenance. Hypoxia-inducible factor-1 (HIF-1) is a decisive element for the transcriptional regulation of genes essential for adaptation to low oxygen conditions. HIF-1 is also implicated in the molecular mechanisms of ageing. Here, we show that the cellular depletion of WRN protein (by siRNA targeting) leads to increased HIF-1 complex stabilization and activation. HIF-1 activation in the absence of WRN involves the generation of mitochondrial reactive oxygen species (mtROS) since SkQ1, a mitochondrial-targeted antioxidant, and stigmatellin, an inhibitor of mitochondrial complex III, blocked increased HIF-1 levels. Ascorbate, an essential co-factor involved in HIF-1 stability, was decreased in WRN-depleted cells. Interestingly, expression levels of GLUT1, a known dehydroascorbic acid transporter, were also decreased in WRN-depleted cells. Ascorbate supplementation of WRN-depleted cells led to a dose-dependent inhibition of HIF-1 activation. These results indicate that WRN protein regulates HIF-1 activation by affecting mitochondrial ROS production and intracellular ascorbate levels. This work provides a novel mechanistic link between HIF-1 activity and different age-associated pathologies." @default.
• W2091658446 created "2016-06-24" @default.
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• W2091658446 date "2012-08-01" @default.
• W2091658446 modified "2023-10-03" @default.
• W2091658446 title "The Werner syndrome gene product (WRN): a repressor of hypoxia-inducible factor-1 activity" @default.
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• W2091658446 doi "https://doi.org/10.1016/j.yexcr.2012.04.010" @default.
• W2091658446 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22659133" @default.
• W2091658446 hasPublicationYear "2012" @default.
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