Inhibition of a radiation-induced senescence-like phenotype: a possible mechanism for potentially lethal damage repair in vascular endothelial cells.
The well-established process of potentially lethal damage (PLD) repair enhances plateau-phase cell survival after exposure to ionizing radiation. PLD repair requires that confluent cells be incubated prior to plating for a colony-forming assay rather than being plated immediately. Enhanced double-strand break (DSB) repair during this incubation period has been implicated in the enhanced survival, but the precise molecular mechanism and its biological significance remain largely unclear. Radiation has been recently reported to induce premature senescence, and increasing evidence suggests that DSBs commonly mediate cellular senescence. Here we successfully related these two biological phenomena using bovine aortic endothelial cells, and propose that enhanced DSB repair during the plateau-phase incubation prevents expression of the radiation-induced senescence-like phenotype, eventually leading to an enhanced colony-forming ability. This could be a novel biological interpretation of PLD repair.
Igarashi
Kaori
K
Oral Radiation Oncology, Department of Oral Restitution, Graduate School, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8549.
Miura
Masahiko
M
D000818:Animals; D001011:Aorta / Q000166:cytology; D002417:Cattle; D002470:Cell Survival / Q000528:radiation effects; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000502:physiology*; D053903:DNA Breaks, Double-Stranded / Q000528:radiation effects*; D004260:DNA Repair / Q000502:physiology*; D042783:Endothelial Cells / Q000502:physiology / Q000528:radiation effects*; D004730:Endothelium, Vascular / Q000166:cytology*