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

机译:抑制辐射诱导的衰老样表型:修复血管内皮细胞中潜在致死性损伤的可能机制

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摘要

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.
机译:完善的潜在致死性损伤(PLD)修复过程可提高暴露于电离辐射后的平稳期细胞存活率。 PLD修复需要在铺板前先对融合细胞进行培养,以进行集落形成试验,而不是立即铺板。在此潜伏期中增强的双链断裂(DSB)修复与提高的存活率有关,但确切的分子机制及其生物学意义仍不清楚。最近有报道称辐射会诱发过早衰老,越来越多的证据表明DSB通常会介导细胞衰老。在这里,我们成功地使用牛主动脉内皮细胞关联了这两种生物学现象,并提出在平台期孵育过程中增强的DSB修复可防止放射诱导的衰老样表型的表达,最终导致增强的菌落形成能力。这可能是PLD修复的一种新颖的生物学解释。 (C)辐射研究学会,2008年。

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