Controlled induction of DNA double-strand breaks in the mouse liver induces features of tissue ageing
Open accessAbstract
DNA damage has been implicated in ageing, but direct evidence for a causal relationship is lacking, owing to the difficulty of inducing defined DNA lesions in cells and tissues without simultaneously damaging other biomolecules and cellular structures. Here we directly test whether highly toxic DNA double-strand breaks (DSBs) alone can drive an ageing phenotype using an adenovirus-based system based on tetracycline-controlled expression of the SacI restriction enzyme. We deliver the adenovirus to mice and compare molecular and cellular end points in the liver with normally aged animals. Treated, 3-month-old mice display many, but not all signs of normal liver ageing as early as 1 month after treatment, including ageing pathologies, markers of senescence, fused mitochondria and alterations in gene expression profiles. These results, showing that DSBs alone can cause distinct ageing phenotypes in mouse liver, provide new insights in the role of DNA damage as a driver of tissue ageing.
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DSB induction was sufficient to promote a subset of age-related pathologies in mice.
“Consistent with the latter, DSB induction was found to be sufficient to promote a subset of age-related pathologies in mice (4).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [4]
DNA damage-driven inflammatory responses have been linked to aging in several organisms.
“Indeed, DNA damage-driven inflammatory responses have been linked to aging in several organisms (4,21).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [4]
A recent study found that age-associated functional decline from DNA damage is largely due to systemic effects of DSBs, such as cell death, tissue atrophy, and non-cell-autonomous inflammation.
“a recent study shows that DNA damage-induced, age-associated functional decline can be attributed in large part to systemic consequences of DSBs, including cell death, tissue atrophy and the ensuing, non-cell-autonomous inflammatory response (4).”
From Controlled DNA double-strand break induction in mice reveals post-damage transcriptome stability (2016) · cites this paper as [4]
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- Authors
- White, R. R., Milholland, B., de Bruin, A., Curran, S., Laberge, R.-M., van Steeg, H., Campisi, J., Maslov, A. Y., & Vijg, J.
- Affiliations
- Albert Einstein College of Medicine (US)
- Buck Institute for Research on Aging (US)
- Corresponding author
- White, Ryan R.
- Vijg, Jan
- Venue
- Nature Communications
- Published
- 2015-04-10
- Volume
- 6
- Issue
- 1
- Pages
- 6790-6790
- ISSN
- 2041-1723 (ISSN-L)
- PMC
- PMC4394211
- OpenAlex
- W2146010728
- Cited by
- 107
- References
- 63
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 10 · 2023: 16 · 2022: 9 · 2021: 6 · 2020: 6 · 2019: 7 · 2018: 8 · 2017: 16 · 2016: 18 · 2015: 4
- FWCI
- 6.14
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Nature Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- Rivm Repository (Netherlands National Institute for Public Health and the Environment) (submittedVersion)
- Funders
- Ellison Medical Foundation
- Glenn Foundation for Medical Research
- National Institutes of Health (AG17242)
- National Institute on Aging (P30AG038072, P01AG017242)
- National Cancer Institute (P30CA013330)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- DNA double-strand breaks, tissue aging, DNA damage, adenoviral gene transfer, cellular senescence, mitochondrial fusion, gene expression profiling, mouse liver
- MeSH terms
- Adenoviridae, Aging, Animals, DNA, DNA Repair, Gene Expression Regulation, Genetic Vectors, Liver, Male, Mice, Inbred BALB C, Tetracycline, Deoxyribonucleases, Type II Site-Specific, Biomarkers, Transgenes, Gene Expression Profiling, Mice, DNA Breaks, Double-Stranded
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