Gene-Specific DNA Repair of Pyrimidine Dimers Does Not Decline during Cellular Aging in Vitro

A large number of studies have demonstrated that various kinds of DNA damage accumulate during aging and one of the causes for this could be a decrease in DNA repair capacity. However, the level of total genomic repair has not been strongly correlated with aging. DNA repair of certain kinds of damag...

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Bibliographic Details
Published in:Experimental cell research 2000-04, Vol.256 (1), p.308-314
Main Authors: Christiansen, M., Stevnsner, T., Bohr, V.A., Clark, B.F.C., Rattan, S.I.S.
Format: Article
Language:English
Subjects:
Adult
aging
Cells, Cultured
Cellular Senescence - genetics
DHFR
DNA Damage
DNA repair
DNA Repair - genetics
Female
Fibroblasts - cytology
Fibroblasts - physiology
Fibroblasts - radiation effects
Genes, p53
human
Humans
Male
Middle Aged
Osteoblasts - cytology
Osteoblasts - physiology
Osteoblasts - radiation effects
p53
Polymorphism, Restriction Fragment Length
Pyrimidine Dimers - metabolism
Restriction Mapping
Skin - cytology
Telomere - genetics
Tetrahydrofolate Dehydrogenase - genetics
Ultraviolet Rays
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Summary:A large number of studies have demonstrated that various kinds of DNA damage accumulate during aging and one of the causes for this could be a decrease in DNA repair capacity. However, the level of total genomic repair has not been strongly correlated with aging. DNA repair of certain kinds of damage is known to be closely connected to the transcription process; thus, we chose to investigate the level of gene-specific repair of UV-induced damage using in vitro aging of human diploid skin fibroblasts and trabecular osteoblasts as model systems for aging. We find that the total genomic repair is not significantly affected during cellular aging of cultures of both human skin fibroblasts and trabecular osteoblasts. Gene-specific repair was analyzed during cellular aging in the dihydrofolate reductase housekeeping gene, the p53 tumor suppressor gene, and the inactive region X754. There was no clear difference in the capacity of young and old cells to repair UV-induced pyrimidine dimers in any of the analyzed genes. Thus, in vitro senescent cells can sustain the ability to repair externally induced damage.
ISSN:0014-4827
1090-2422
DOI:10.1006/excr.2000.4826