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Expression of Proteins Coincident with Inducible Radioprotection in Human Lung Epithelial Cells¹

Department of Biological Sciences, Brunel University, Uxbridge, Middlesex, UB8 3PH [S. C. G., A. A-P., J. E. A.]; Department of Cardiothoracic Surgery, National Heart and Lung Institute, Imperial College School of Medicine, Heart Science Centre, Harefield Hospital, Harefield, Middlesex, UB9 6JH [M. J. D., C. H. W.]; and Gray Laboratory, Mount Vernon Hospital, Northwood, Middlesex, HA6 2JR [M. C. J.], United Kingdom

Human lung epithelial cells and many other cell lines are hypersensitive to low doses of ionizing radiation (<0.2 Gy). However, above a threshold dose of 0.4–0.6 Gy, an induced radioprotective response is triggered that protects cells at higher radiation doses. At 4 h, when maximal induced radioprotection is seen in these cells after low-dose priming, the two-dimensional gel protein expression pattern in 0.5-Gy-exposed cells is subtly altered, with seven proteins being 2- to 5-fold down-regulated and one being 2-fold up-regulated. They include: (a) the protein kinase C inhibitor 1, or histidine triad nucleotide-binding motif (HINT) protein; (b) substrates for protein kinase C activity including the chloride intracellular channel protein 1; and (c) a cytoskeletal protein degraded during apoptosis. In addition, a lung cancer-specific protein that binds to both telomeres and nascent mRNA molecules is down-regulated, as is interleukin 1. Therefore, at least in human lung epithelial cells, radioprotection may be the result of signaling pathway switching, which results in the removal of damaged cells and the preparation for enhanced general transcription in surviving cells during a period in which cell proliferation is repressed. This combination of events may be cell-type-specific and may have implications for the protection of normal lung tissue during unavoidable radiation exposure such as in radiotherapy.