Repeated exposure of human fibroblasts to ionizing radiation reveals an adaptive response that is not mediated by interleukin-6 or TGF-<tex>$\beta$</tex>
Faculty of Pharmaceutical, Biomedical and Veterinary Sciences . Biomedical Sciences
Engineering sciences. Technology
Mutation research: international journal on mutagenesis, chromosome breakage and related subjects. - Amsterdam
, p. 19-24
Exposing cells to a low dose can protect them against a subsequent higher exposure. This phenomenon is known as adaptive response and is frequently observed in a variety of cells. Even though similarities are suspected with other non-targeted effects, such as bystander effects, the exact mechanism behind adaptive response is not fully clarified. In this study human primary fibroblasts were tested for their response to ionizing radiation (IR) after administrating a low priming dose (0.1-0.5 Gy). Both the abundance of gamma H2AX as a marker for double-stranded breaks and the levels of cytokines, secreted in the medium, were monitored in time. Upon challenge, IR-primed cells showed modified gamma H2AX spot size distributions and altered repair kinetics, consistent with an adaptive response. In addition, 24 h after priming with IR, four cytokines were significantly upregulated in the medium - GM-CSF (1.33 x); IL6 (4.24 x); IL8 (1.33x); TGF-beta (1.46x). In order to mimick the protective effect of IR priming, we primed the cells with either IL6 or TGF-beta. This did not elicit an altered gamma H2AX response as observed in IR-primed cells, indicating that the adaptive response in these primary fibroblasts is regulated in an IL-6 and TGF-beta independent manner. (C) 2011 Elsevier B.V. All rights reserved.