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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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Items 101–166 of 166
Saha, B., Pallatt, S., Banerjee, A., Banerjee, A. G., Pathak, R., & Pathak, S. (2024) · Cells · doi:10.3390/cells13181560 · Cited by 20
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“High doses of radiation may induce responses such as oxidative stress, cellular senescence, and the activation of genes which are linked to aging (19, 20).”
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“When bone marrow is subjected to a high dose, there is an increase in expression of the ageing and senescent cell biomarker p16 INK4a (Le et al., 2010; Bork et al., 2010) reducing the capacity for stem cell renewal and, consequently, causing a decline in cellularity commensurate with premature ageing (Barranco et al.,…”
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“It can be triggered by various stresses, such as inflammatory stress (Paramos- de-Carvalho et al., 2021 ), oxidative stress (Chen et al., 1995), chemotherapy (Schmitt et al., 2002 ), and irradiation (Le et al., 2010 ).”
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“Previously reported studies have shown that senescence of hematopoietic stem cells is induced by TBI (61, 62) and is expressed long after irradiation (63).”
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“CDKIs are keys to regulate cell cycle (Le et al., 2010).”
BackgroundSustained p16INK4a expression is required to prevent IR-induced tumorigenesis in mice
Palacio, L., Krishnan, V., Le, N. L. O., Sharpless, N. E., & Beausejour, C. M. (2016) · Oncogene · doi:10.1038/onc.2016.298 · Cited by 7
“We had previously performed time course studies and found that a minimum of 6–8 weeks is necessary to observe robust IR-induced p16 INK4a expression in mouse tissues 16 .”
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“Although 53BP1-positive cells declined spontaneously, their elevation persisted for at least 45 weeks compared with that in the controls [94].”
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“Exposure to IR induces long-term persistent senescence status in different cell lines that contributes to reduced functionality of the affected tissues [70].”
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The Immunogenicity of Human Senescent Cells Is Dependent on the Senescence Inducer and Cell Type
Goyer, M., Sonn, A., Benabdallah, B., Lê, O., Dulong, J., Oschwald, J., Sirois, I., Apavaloaei, A., Hesnard, L., Guimond, J. V., et al. (2026) · Aging Cell · doi:10.1111/acel.70410 · Cited by 4
“In contrast, senescent cells in a nevus or induced by ionizing radiation (IR) display no signs of immune clearance (Le et al. 2010; Michaloglou et al. 2005).”
Goyer, M., Désaulniers-Langevin, C., Sonn, A., Nehmo, G. M., Lisi, V., Benabdallah, B., Raynal, N. J. ‐., & Beausejour, C. M. (2024) · Cells · doi:10.3390/cells13100849 · Cited by 4
“In contrast, p16 often responds to DNA damage in a delayed manner [20,21].”
BackgroundInfluentialKiller, K., Lê, O., & Beausejour, C. M. (2021) · Radiation Research · doi:10.1667/rade-21-00017.1 · Cited by 4
Zhang, L., Cai, L., Cai, Y., Ke, W., Zhou, L., Yang, Y. S., Huang, W., Zou, J., & Chen, H. (2024) · International Journal of Radiation Biology · doi:10.1080/09553002.2024.2404456 · Cited by 3
“…Le et al. who detected a significant increase in the proportion of cells positive for the DNA damage marker 53BP1 in C57BL/6J mice at 24 h after 8 Gy irradiation and a gradual decrease over time, but still significant higher than the control group up to 45 weeks after irradiation (Le et al. 2010).”
Maier, I., Ruegger, P. M., Deutschmann, J., Helbich, T. H., Pietschmann, P., Schiestl, R. H., & Borneman, J. (2021) · Radiation Research · doi:10.1667/rade-21-00065.1 · Cited by 3
“Moreover, ionizing radiation aggravates osteogenic differentiation dysfunction and the expression of senescence markers independent of tumor suppressor gene p53 (18).”
BackgroundTargeting Senescent Cells to Improve Human Health
Wijshake, T., & van Deursen, J. M. A. (2016) · Healthy ageing and longevity · doi:10.1007/978-3-319-26239-0_16 · Cited by 3
“The mechanisms underlying these cancertherapy associated disabilities are not well understood, but it seems likely that the induction of senescent cells due to DNA-damaging therapies is contributing to the long-term complications after cancer therapy (Roninson 2003; Le et al. 2010).”
BackgroundLee, J., Chen, X., Fanning, K. M., Si, C., Davis, A., Wasserman, D. H., Bracy, D. P., Furdui, C. M., & Kavanagh, K. (2025) · Radiation Research · doi:10.1667/rade-23-00223.1 · Cited by 2
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ZNF768 loss amplifies p53 action and reduces lung tumorigenesis in mice
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“It combines immunofluorescence for DNA damage response factors (e.g. 53BP1) (Le et al., 2010) and FISH against telomeric DNA.”
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Heath, J. (2018) · Memorial University Research Repository (Memorial University)
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Chronically disrupted sleep induces senescence in the visceral adipose tissue of C57BL/6 micePreprint
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Brain irradiation drives remote liver changes via senescence-independent mechanisms
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“Based on the literature, this study employed single dose of 0.1 Gy, 0.2 Gy and 0.5 Gy administered every 48 hours for a total of 16 times, with group settings of the 0.1 Gy × 16, the 0.2 Gy × 16 and the 0.5 Gy × 16, respectively [5, 31–34].”
Influential
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
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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