4.4 Article

Inhibition of a radiation-induced senescence-like phenotype: A possible mechanism for potentially lethal damage repair in vascular endothelial cells

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RADIATION RESEARCH
卷 170, 期 4, 页码 534-539

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RADIATION RESEARCH SOC
DOI: 10.1667/RR1423.1

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  1. Ministry of Education, Culture, Sports, Science and Technology of Japan
  2. Toyo Suisan, Co. Ltd
  3. Takamatsu Cancer Research Fund

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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. (C) 2008 by Radiation Research Society.

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