Mechanisms of the elimination of low dose hyper-radiosensitivity in T-47D cells by low dose-rate priming

Edin, Nina Frederike Jeppesen; Olsen, Dag Rune; Stokke, Trond; Sandvik, Joe Alexander; Ebbesen, Peter; Pettersen, Erik O.

doi:10.3109/09553000903242107

Cited by 11 publications

(25 citation statements)

References 20 publications

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“…From previous experiments, it was known that the presence of serum was essential for LDR irradiation to have an effect on HRS [10]. In order to identify the factor required in the serum, interleukins 4 and 13 were tested on both T-47D cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…The culture conditions were as described previously [4, 10, 19] using RPMI1640 (Roswell Park Memorial Institute) medium (JRH Biosciences, Kansas, USA) supplemented with 10% fetal calf serum (Gibco, Paisley, UK), 2 mM L-glutamine (SIGMA, St Louis, MO , USA), 200 units l −1 insulin (SIGMA), and 1% C. The cells were kept in exponential growth by reculturing of stock cultures two times a week. The cells were tested negative for the presence of mycoplasma.…”

Section: Methodsmentioning

confidence: 99%

“…Within each experiment, the arithmetic means were calculated, weighing the errors. Radiation survival curve data were fitted using the linear quadratic (LQ) or the induced repair (IR) model [4, 10, 19]. …”

Section: Methodsmentioning

confidence: 99%

“…However, in cells that were LDR irradiated themselves, the HRS-response was removed permanently. Both the mechanism that induced the non-HRS response and the mechanism maintaining the non-HRS response were found to depend on iNOS activation and peroxynitrite generation from nitric oxide (NO) and superoxide [9, 10]. …”

Section: Introductionmentioning

confidence: 99%

“…Also, the removal of HRS in cells receiving LDR-irradiated cell conditioned medium depended on the presence of serum during conditioning of the medium, but not during LDR irradiation [10]. …”

Section: Introductionmentioning

confidence: 99%

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The role of interleukin-13 in the removal of hyper-radiosensitivity by priming irradiation

Edin

2014

Journal of Radiation Research

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It has previously been demonstrated that the presence of fetal bovine serum is necessary for TGF-β3 (transforming growth factor beta 3)-dependent elimination of low-dose hyper-radiosensitivity (HRS) in cells by 1 h of low-dose-rate γ-irradiation (0.2–0.3 Gy/h). The purpose of the present study was to identify the serum constituent involved. Two human HRS-positive (T-47D, T98G) cell lines were used. The effects of different pretreatments on HRS were investigated using the colony assay. Total inducible nitric oxide synthase (iNOS) levels were measured using a cell-based ELISA assay. The serum factor was identified as interleukin-13 (IL-13). In order for low dose-rate irradiation to eliminate HRS through the TGF-β3-dependent mechanism, the cells must be exposed to IL-13 first. Inhibiting receptor IL-13Rα2 showed that this receptor is involved in the response. Adding IL-13 to serum-free medium restored the properties of full medium but not when an inhibitor of proprotein convertase activity was added together with IL-13. The presence of IL-13 resulted in upregulation of total iNOS protein levels. Thus, this study indicates that IL-13 interacts with the cells though receptor IL-13Rα2 and induces upregulation of iNOS and activation of one or more furin-like proprotein convertases.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The role of interleukin-13 in the removal of hyper-radiosensitivity by priming irradiation

Edin

2014

Journal of Radiation Research

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Datasets of in vitro clonogenic assays showing low dose hyper-radiosensitivity and induced radioresistance

2022

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Low dose hyper-radiosensitivity and induced radioresistance are primarily observed in surviving fractions of cell populations exposed to ionizing radiation, plotted as the function of absorbed dose. Several biophysical models have been developed to quantitatively describe these phenomena. However, there is a lack of raw, openly available experimental data to support the development and validation of quantitative models. The aim of this study was to set up a database of experimental data from the public literature. Using Google Scholar search, 46 publications with 101 datasets on the dose-dependence of surviving fractions, with clear evidence of low dose hyper-radiosensitivity, were identified. Surviving fractions, their uncertainties, and the corresponding absorbed doses were digitized from graphs of the publications. The characteristics of the cell line and the irradiation were also recorded, along with the parameters of the linear-quadratic model and/or the induced repair model if they were provided. The database is available in STOREDB, and can be used for meta-analysis, for comparison with new experiments, and for development and validation of biophysical models.

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Integrated Modelling of Cell Responses after Irradiation for DNA-Targeted Effects and Non-Targeted Effects

Matsuya

Sasaki

Yoshii

et al. 2018

Sci Rep

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Intercellular communication after ionizing radiation exposure, so-called non-targeted effects (NTEs), reduces cell survival. Here we describe an integrated cell-killing model considering NTEs and DNA damage along radiation particle tracks, known as DNA-targeted effects (TEs) based on repair kinetics of DNA damage. The proposed model was applied to a series of experimental data, i.e., signal concentration, DNA damage kinetics, cell survival curve and medium transfer bystander effects (MTBEs). To reproduce the experimental data, the model considers the following assumptions: (i) the linear-quadratic (LQ) function as absorbed dose to express the hit probability to emit cell-killing signals, (ii) the potentially repair of DNA lesions induced by NTEs, and (iii) lower efficiency of repair for the damage in NTEs than that in TEs. By comparing the model results with experimental data, we found that signal-induced DNA damage and lower repair efficiency in non-hit cells are responsible for NTE-related repair kinetics of DNA damage, cell survival curve with low-dose hyper-radiosensitivity (HRS) and MTBEs. From the standpoint of modelling, the integrated cell-killing model with the LQ relation and a different repair function for NTEs provide a reasonable signal-emission probability and a new estimation of low-dose HRS linked to DNA repair efficiency.

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Mechanisms of the elimination of low dose hyper-radiosensitivity in T-47D cells by low dose-rate priming

Abstract: LDR priming of T-47D cells as well as LDR priming of medium conditioned on T-47D cells induce a factor in the medium which cause the early G(2)-checkpoint to be activated in recipient cells by doses normally in the HRS dose-range.

Cited by 11 publications

References 20 publications

The role of interleukin-13 in the removal of hyper-radiosensitivity by priming irradiation

The role of interleukin-13 in the removal of hyper-radiosensitivity by priming irradiation

Datasets of in vitro clonogenic assays showing low dose hyper-radiosensitivity and induced radioresistance

Integrated Modelling of Cell Responses after Irradiation for DNA-Targeted Effects and Non-Targeted Effects

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