Document Detail

Cells from long-lived mutant mice exhibit enhanced repair of ultraviolet lesions.
MedLine Citation:
PMID:  18375871     Owner:  NLM     Status:  MEDLINE    
Fibroblasts isolated from long-lived hypopituitary dwarf mice are resistant to many cell stresses, including ultraviolet (UV) light and methyl methane sulfonate (MMS), which induce cell death by producing DNA damage. Here we report that cells from Snell dwarf mice recover more rapidly than controls from the inhibition of RNA synthesis induced by UV damage. Recovery of messenger RNA (mRNA) synthesis in particular is more rapid in dwarf cells, suggesting enhanced repair of the actively transcribing genes in dwarf-derived cells. At early time points, there was no difference in the repair of cyclobutane pyrimidine dimers (CPD) or 6-4 photoproducts (6-4PP) in the whole genome, nor was there any significant difference in the repair of UV lesions in specific genes. However, at later time points we found that more lesions had been removed from the genome of dwarf-derived cells. We have also found that cells from dwarf mice express higher levels of the nucleotide excision repair proteins XPC and CSA, suggesting a causal link to enhanced DNA repair. Overall, these data suggest a mechanism for the UV resistance of Snell dwarf-derived fibroblasts that could contribute to the delay of aging and neoplasia in these mice.
Adam B Salmon; Mats Ljungman; Richard A Miller
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  The journals of gerontology. Series A, Biological sciences and medical sciences     Volume:  63     ISSN:  1079-5006     ISO Abbreviation:  J. Gerontol. A Biol. Sci. Med. Sci.     Publication Date:  2008 Mar 
Date Detail:
Created Date:  2008-03-31     Completed Date:  2008-06-06     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  9502837     Medline TA:  J Gerontol A Biol Sci Med Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  219-31     Citation Subset:  AIM; IM    
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MeSH Terms
Blotting, Western
Cells, Cultured
DNA / chemistry,  genetics
DNA Damage
DNA Repair*
DNA-Binding Proteins / metabolism
Dwarfism, Pituitary / genetics,  pathology
Endonucleases / metabolism
Enzyme-Linked Immunosorbent Assay
Fibroblasts / cytology,  metabolism*,  radiation effects*
Mice, Inbred C3H
Mice, Inbred Strains
Mice, Mutant Strains
Nuclear Proteins / metabolism
Pyrimidine Dimers / analysis,  chemistry
RNA, Messenger / genetics,  metabolism
Time Factors
Transcription Factors / metabolism
Ultraviolet Rays*
Grant Support
AG023122/AG/NIA NIH HHS; AG054624/AG/NIA NIH HHS; T32 AG000114/AG/NIA NIH HHS; T32 AG000114-24/AG/NIA NIH HHS; T32-AG000114/AG/NIA NIH HHS; U19 AG023122/AG/NIA NIH HHS; U19 AG023122-05/AG/NIA NIH HHS
Reg. No./Substance:
0/DNA excision repair protein ERCC-5; 0/DNA-Binding Proteins; 0/Nuclear Proteins; 0/Pyrimidine Dimers; 0/RNA, Messenger; 0/Transcription Factors; 0/xeroderma pigmentosum group F protein; 9007-49-2/DNA; EC 3.1.-/Endonucleases

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