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Ionizing radiation-induced long-term expression of senescence markers in mice is independent of p53 and immune status
Open accessAbstract
Exposure to IR has been shown to induce the formation of senescence markers, a phenotype that coincides with lifelong delayed repair and regeneration of irradiated tissues. We hypothesized that IR-induced senescence markers could persist long-term in vivo, possibly contributing to the permanent reduction in tissue functionality. Here, we show that mouse tissues exposed to a sublethal dose of IR display persistent (up to 45 weeks, the maximum time analyzed) DNA damage foci and increased p16(INK4a) expression, two hallmarks of cellular senescence and aging. BrdU-labeling experiments revealed that IR-induced damaged cells are preferentially eliminated, at least partially, in a tissue-dependent manner. Unexpectedly, the accumulation of damaged cells was found to occur independent from the DNA damage response modulator p53, and from an intact immune system, as their levels were similar in wild-type and Rag2(-/-) gammaC(-/-) mice, the latter being deficient in T, B, and NK cells. Together, our results provide compelling evidence that exposure to IR induces long-term expression of senescence markers in vivo, an effect that may contribute to the reduced tissue functionality observed in cancer survivors.
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“Ageing and genotoxic stress induce cellular senescence of these stem cells 96,97 and osteoprogenitor cells, 98,99 with subsequent decline in the functions of these cells in both mice and humans.100”
From The costs and benefits of senotherapeutics for human health (2022) · cites this paper as [97]
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Self-citation
Metadata
- Authors
- Le, O. N. L., Rodier, F., Fontaine, F., Coppe, J., Campisi, J., DeGregori, J., Laverdière, C., Kokta, V., Haddad, E., & Beauséjour, C. M.
- Affiliations
- Buck Institute for Research on Aging (US)
- University of Colorado Anschutz (US)
- Centre Hospitalier Universitaire Sainte-Justine (CA)
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2010-05-18
- Volume
- 9
- Issue
- 3
- Pages
- 398-409
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC2894262
- OpenAlex
- W1489456875
- Cited by
- 168
- References
- 60
- Citations by year
- 2026: 7 · 2025: 8 · 2024: 14 · 2023: 9 · 2022: 9 · 2021: 22 · 2020: 11 · 2019: 14 · 2018: 8 · 2017: 12 · 2016: 7 · 2015: 10 · 2014: 11 · 2013: 10 · 2012: 6
- FWCI
- 5.56
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Buck Institute for Research on Aging
- National Institutes of Health
- Canadian Institutes of Health Research (IAO-79317)
- National Institute on Aging (R56AG009909, AG017242, AG-09909, R37AG009909, P30AG025708, AG025708, P01AG017242)
- National Cancer Institute (CA12654, R01CA109657, U24CA126546, CA109657)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- ionizing radiation, cellular senescence, DNA damage foci, p16INK4a, immunodeficiency, Rag2 knockout mice, tissue regeneration, sublethal irradiation, cancer survivors, aging, DNA damage response
- MeSH terms
- Adolescent, Animals, B-Lymphocytes, Child, DNA Damage, Humans, Killer Cells, Natural, Mice, Inbred C57BL, Radiation, Ionizing, T-Lymphocytes, Time Factors, Biomarkers, Tumor Suppressor Protein p53, Cellular Senescence, Cyclin-Dependent Kinase Inhibitor p16, Mice
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