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Abstract
Purpose: Radiation-induced adaptive response (AR) is a phenomenon of increased radioresistance mediated by a low priming dose of ionizing radiation (IR) applied prior to a higher challenging dose. We have previously shown that in mouse-embryo fibroblasts (MEF) and human A549 cells, AR is associated with enhanced repair of DNA double-strand breaks (DSB) by the DNA-PK-dependent pathway of non-homologous end-joining (D-NHEJ). Importantly, AR was ‘transmitted’ to non-irradiated bystander cells through transfer of medium from cells that had received a priming dose of IR. Here, we examine the influence of the genetic background in these responses.
Materials and methods: Two plasmid-based assays specifically designed to measure the efficiency of NHEJ and HRR (homologous recombination repair) were deployed. MEF and the primary human fibroblast cell lines HF12 and HF19 were exposed to 10 mGy to 5 Gy X-rays. Bystander effects were investigated using the medium-transfer technique.
Results: In contrast to MEF, which induce robust AR to NHEJ, even as a bystander response, human fibroblasts fail to develop such phenomena.
Conclusions: The development of AR is cell-type-specific. The same holds true for the development of AR as a bystander effect. Better understanding of the underlying mechanisms will help to understand the molecular basis of these differences in response.
Acknowledgements
This study was supported by a grant (NOTE: 036465-FI6R) from the European Union Sixth Framework Programme. We thank Dr Fred Alt for cells and Drs Vera Gorbunova and Robert Schiestl for plasmids.
Declaration of interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.