title: Introduction of human telomerase reverse transcriptase to normal human fibroblasts enhances DNA repair capacity.
abstract: OBJECTIVE
  From numerous reports on proteins involved in DNA repair and telomere maintenance that physically associate with human telomerase reverse transcriptase (hTERT), we inferred that hTERT/telomerase might play a role in DNA repair. We investigated this possibility in normal human oral fibroblasts (NHOF) with and without ectopic expression of hTERT/telomerase.
  
  
  METHODS
  To study the effect of hTERT/telomerase on DNA repair, we examined the mutation frequency rate, host cell reactivation rate, nucleotide excision repair capacity, and DNA end-joining activity of NHOF and NHOF capable of expressing hTERT/telomerase (NHOF-T). NHOF-T was obtained by transfecting NHOF with hTERT plasmid.
  
  
  RESULTS
  Compared with parental NHOF and NHOF transfected with empty vector (NHOF-EV), we found that (a) the N-methyl-N'-nitro-N-nitrosoguanidine-induced mutation frequency of an exogenous shuttle vector was reduced in NHOF-T, (b) the host cell reactivation rate of N-methyl-N'-nitro-N-nitrosoguanidine-damaged plasmids was significantly faster in NHOF-T; (c) the nucleotide excision repair of UV-damaged DNA in NHOF-T was faster, and (d) the DNA end-joining capacity in NHOF-T was enhanced. We also found that the above enhanced DNA repair activities in NHOF-T disappeared when the cells lost the capacity to express hTERT/telomerase.
  
  
  CONCLUSIONS
  These results indicated that hTERT/telomerase enhances DNA repair activities in NHOF. We hypothesize that hTERT/telomerase accelerates DNA repair by recruiting DNA repair proteins to the damaged DNA sites.
authors.affiliation: School of Dentistry, University of California, Los Angeles, California 90095, USA.
authors.forename: Ki-Hyuk
authors.initials: KH
authors.lastname: Shin
authors.forename: Mo K
authors.initials: MK
authors.lastname: Kang
authors.forename: Erica
authors.initials: E
authors.lastname: Dicterow
authors.forename: Ayako
authors.initials: A
authors.lastname: Kameta
authors.forename: Marcel A
authors.initials: MA
authors.lastname: Baluda
authors.forename: No-Hee
authors.initials: NH
authors.lastname: Park
mesh_terms: D015139:Blotting, Southern; D002478:Cells, Cultured; D004247:DNA / Q000737:chemistry / Q000378:metabolism; D004249:DNA Damage; D004252:DNA Mutational Analysis; D004260:DNA Repair; D004268:DNA-Binding Proteins; D004307:Dose-Response Relationship, Radiation; D005347:Fibroblasts / Q000378:metabolism*; D006801:Humans; D008156:Luciferases / Q000378:metabolism; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology; D009154:Mutation; D012333:RNA, Messenger / Q000378:metabolism; D019098:Telomerase / Q000378:metabolism*; D014162:Transfection; D014466:Ultraviolet Rays
chemical_list: D004268:DNA-Binding Proteins; D012333:RNA, Messenger; D008769:Methylnitronitrosoguanidine; D004247:DNA; D008156:Luciferases; D019098:Telomerase