Chronic Oxidative Stress Compromises Telomere Integrity and Accelerates the Onset of Senescence in Human Endothelial Cells
Open accessAbstract
Replicative senescence and oxidative stress have been implicated in ageing, endothelial dysfunction and atherosclerosis. Replicative senescence is determined primarily by telomere integrity. In endothelial cells the glutathione redox-cycle plays a predominant role in the detoxification of peroxides. The aim of this study was to elucidate the role of the glutathione-dependent antioxidant system on the replicative capacity and telomere dynamics of cultured endothelial cells. Human umbilical vein endothelial cells were serially passaged while exposed to regular treatment with 0.1 μM tert-butyl hydroperoxide, a substrate of glutathione peroxidase, or 10 μM L-buthionine-[S,R]-sulphoximine, an inhibitor of glutathione synthesis. Both treatments induced intracellular oxidative stress but had no cytotoxic or cytostatic effects. Nonetheless, treated cultures entered senescence prematurely (30 versus 46 population doublings), as determined by senescence-associated β-galactosidase staining and a sharp decrease in cell density at confluence. In cultures subjected to oxidative stress terminal restriction fragment (TRF) analysis demonstrated faster telomere shortening (110 versus 55 bp/population doubling) and the appearance of distinct, long TRFs after more than 15-20 population doublings. Fluorescence in situ hybridisation analysis of metaphase spreads confirmed the presence of increased telomere length heterogeneity, and ruled out telomeric end-to-end fusions as the source of the long TRFs. The latter was also confirmed by Bal31 digestion of genomic DNA. Similarly, upregulation of telomerase could not account for the appearance of long TRFs, as oxidative stress induced a rapid and sustained decrease in this activity. These findings demonstrate a key role for glutathione-dependent redox homeostasis in the preservation of telomere function in endothelial cells and suggest that loss of telomere integrity is a major trigger for the onset of premature senescence under mild chronic oxidative stress.
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Inhibiting or reducing GSH synthesis is sufficient to induce premature senescence and OS-mediated telomere shortening in HUVEC, and this condition is not restored by telomerase activity.
“For example, inhibiting or reducing GSH synthesis is sufficient to induce premature senescence and OS-mediated telomere shortening in HUVEC, and this condition is not restored by telomerase activity [187].”
From The Role of Antioxidants in the Interplay between Oxidative Stress and Senescence (2022) · cites this paper as [187]
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- Authors
- Kurz, D. J., Decary, S., Hong, Y., Trivier, E., Akhmedov, A., & Erusalimsky, J. D.
- Affiliations
- University of Zurich (CH)
- Department of Medicine, University College London, 5 University Street, London, WC1E 6JF, UK
- University College London (GB)
- Corresponding author
- Erusalimsky, Jorge D.
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2004-05-01
- Volume
- 117
- Issue
- 11
- Pages
- 2417-2426
- ISSN
- 0021-9533 (ISSN-L)
- 1477-9137
- OpenAlex
- W1990423201
- Cited by
- 499
- References
- 56
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 12 · 2023: 19 · 2022: 23 · 2021: 30 · 2020: 16 · 2019: 32 · 2018: 30 · 2017: 22 · 2016: 24 · 2015: 25 · 2014: 37 · 2013: 23 · 2012: 22
- FWCI
- 12.54
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- public-domain
- Locations
- Journal of Cell Science (publishedVersion, public-domain)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- HighWire Press Open Archive (submittedVersion)
- Cardiff Metropolitan Research Repository (Cardiff Metropolitan University) (submittedVersion)
- Funders
- National Science Foundation
- British Heart Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Schweizerische Herzstiftung
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- oxidative stress, replicative senescence, telomere integrity, telomere shortening, endothelial cells, glutathione redox cycle, glutathione peroxidase, tert-butyl hydroperoxide, telomere length heterogeneity, telomerase, premature senescence, aging, endothelial dysfunction, atherosclerosis
- MeSH terms
- Cell Cycle, Cell Line, Enzyme Inhibitors, Glutamate-Cysteine Ligase, Humans, Down-Regulation, Telomere, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Telomerase, Buthionine Sulfoximine, tert-Butylhydroperoxide, Endothelial Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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