ArticleAging2019
Delayed γH2AX foci disappearance in mammary epithelial cells from aged women reveals an age-associated DNA repair defect.
Article in Aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Role of H4K16 acetylation in 53BP1 recruitment to double-strand break sites in in vitro aged cells.Biogerontology · 2022Article
- Chemotherapeutic Drug-Regulated Cytokines Might Influence Therapeutic Efficacy in HCC.International journal of molecular sciences · 2021Review
- Sex-specific differences in DNA double-strand break repair of cycling human lymphocytes during aging.Aging · 2021Article
- DeepFoci: Deep learning-based algorithm for fast automatic analysis of DNA double-strand break ionizing radiation-induced foci.Computational and structural biotechnology journal · 2021Article
- Article
- Polymorphisms in XPC Gene and Risk of Uterine Leiomyoma in Reproductive Women.Pathology oncology research : POR · 2020Article
- Estrogen Induces Mammary Ductal Dysplasia via the Upregulation of Myc Expression in a DNA-Repair-Deficient Condition.iScience · 2020Article
- STRIDE-a fluorescence method for direct, specific in situ detection of individual single- or double-strand DNA breaks in fixed cells.Nucleic acids research · 2020Article
- Salusin-β mediates tubular cell apoptosis in acute kidney injury: Involvement of the PKC/ROS signaling pathway.Redox biology · 2020Article
- Inverse dose-rate effect of ionising radiation on residual 53BP1 foci in the eye lens.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a degenerative process in which genome instability plays a crucial role. To gain insight into the link between organismal aging and DNA repair capacity, we analyzed DNA double-strand break (DSB) resolution efficiency in human mammary epithelial cells from 12 healthy donors of young and old ages. The frequency of DSBs was measured by quantifying the number of γH2AX foci before and after 1Gy of γ-rays and it was higher in cells from aged donors (ADs) at all times analyzed. At 24 hours after irradiation, ADs retained a significantly higher frequency of residual DSBs than young donors (YDs), which had already reached values close to basal levels. The kinetics of DSB induction and disappearance showed that cells from ADs and YDs repair DSBs with similar speed, although analysis of early times after irradiation indicate that a repair defect may lie within the firing of the DNA repair machinery in AD cells. Indeed, using a mathematical model we calculated a constant factor of delay affecting aged human epithelial cells repair kinetics. This defect manifests with the accumulation of DSBs that might eventually undergo illegitimate repair, thus posing a relevant threat to the maintenance of genome integrity in older individuals.
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Registered trials
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