What role for DNA damage and repair in the bystander response?

Prise, Kevin M.; Folkard, M.; Kuosaite, Virginija; Tartier, Laurence; Zyuzikov, Nikolai; Shao, Chunlin

doi:10.1016/j.mrfmmm.2005.06.034

Cited by 42 publications

(25 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This now well accepted phenomenon, called the bystander effect, has been reported in various cell types and biological endpoints such as sister chromatid exchange (1, 2), clonogenic survival (3,4), micronucleus formation (5-10), chromatin damage (11), chromosome aberrations (12), foci formation (5), apoptosis (13) etc (for an overview see reviews (14)(15)(16)(17)(18)(19)(20)(21) and summaries (22,23)). Two major mechanisms are described in the literature.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Lack of Bystander Effects from High-LET Radiation for Early Cytogenetic End Points

2008

View full text Add to dashboard Cite

1 Groesser, T., Cooper, B. and Rydberg, B. Lack of Bystander Effects From High LET Radiation ForEarly Cytogenetic Endpoints. Radiat. Res.The aim of this work was to study radiation induced bystander effects for early cytogenetic endpoints in various cell lines using the medium transfer technique after high and low LET radiation. Cells were exposed to 20MeV/amu Nitrogen ions, 968 MeV/amu Iron ions or 575 MeV/amu Iron ions followed by transfer of the conditioned medium from the irradiated cells to unirradiated test cells. The effects studied included DNA double-strand break induction, γ-H2AX foci formation, induction of chromatid breaks in prematurely condensed chromosomes, and micronuclei formation using DNA repair proficient and deficient hamster and human cell lines (xrs6, V79, SW48, MO59K and MO59J). Cell survival was also measured in SW48 bystander cells using X-rays. Although it was possible to occasionally detect an increase in chromatid break levels using Nitrogen ions and seeing a higher number of γ-H2AX foci formation using Nitrogen and Iron ions in xrs6 bystander cells in single experiments, the results were not reproducible. After pooling all the data, we could not verify a significant bystander effect for any these endpoints. Also, we did not detect a significant bystander effect for DSB induction or micronuclei formation in these cell lines or for clonogenic survival in SW48 cells.The data suggest that DNA damage and cytogenetic changes are not induced in bystander cells. In contrast, literature data show pronounced bystander effects in a variety of cell lines, including clonogenic survival in SW48 cells and induction of chromatid breaks and micronuclei in hamster cells. To reconcile these conflicting data, it seems possible that the epigenetic status of the specific cell line or the precise culture conditions and medium supplements, such as serum, might be critical for inducing bystander effects. 2 INTRODUCTIONFor decades it has been a central dogma in radiation biology that the energy from ionizing radiation must be deposited in the cell nucleus of the affected cell or at least in the cell's cytoplasm to induce a radiation response.However, in the last years data have provided evidence that cells that are not hit directly by ionizing radiation are also influenced by damaged neighboring cells. This now well accepted phenomenon, called the bystander effect, has been reported in various cell types and biological endpoints such as sister chromatid exchange (1, 2), clonogenic survival (3, 4), micronucleus formation (5-10), chromatin damage (11), chromosome aberrations (12), foci formation (5), apoptosis (13) etc (for an overview see reviews (14-21) and summaries (22,23)). Two major mechanisms are described in the literature. First a transfer of factors through gap junctions (6) and second a medium mediated transport of the bystander factors independent of cell-cell contact (3,24). However, the factors that are involved in the transmission of the effects are still unknown. Due to the fact that the bystan...

show abstract

Section: Introductionmentioning

confidence: 99%

“…However, the factors that are involved in the transmission of the effects are still unknown. Due to the fact that the bystander effect can be detected at very low doses (see (20) for a review) this phenomenon is important for radiation risk assessment at doses below 1 Gy (overview (14,15,21)). …”

Section: Introductionmentioning

confidence: 99%

Lack of Bystander Effects from High-LET Radiation for Early Cytogenetic End Points

2008

View full text Add to dashboard Cite

show abstract

“…Confirmatory studies found that the production of DNA damage does not trigger the RIBE, but DNA damage and repair proficiency play an important role in the bystander cells. 14,15 At the molecular level, histone H2AX phosphorylation on serine 139 (γ-H2AX) has been shown to be one of the earliest cellular responses to DNA DSB formation. [16][17][18] An assay based on counting the number of discrete subnuclear γ-H2AX foci, each containing a single DNA DSB, 19 has proven to be the most sensitive technique available to evaluate γ-H2AX in Bystander Cells DNA DSB incidence in mammalian cells and tissues.…”

Section: Introductionmentioning

confidence: 99%

γH2AX in Bystander Cells: Not Just a Radiation-Triggered Event, a Cellular Response to Stress Mediated by Intercellular Communication

Sokolov¹,

Dickey²,

Bonner³

et al. 2007

Cell Cycle

View full text Add to dashboard Cite

“…Using precision micro beams, low-dose internal radiation β-particles and hadron radiations, various investigators were able to find out several end-points and effects of bystander signaling in naïve mammalian cells. These include but are not limited to genetic and epigenetic transformations that according to some estimates were previously underestimated [9], genomic instability [10] which can cause lethal mutations and altered gene expression [11], activation of several signal transduction pathways in a dose dependent manner [6,12,13], γ-H 2 AX foci formation [14], delayed apoptosis [1,[15][16][17], sister chromatid exchanges (SCE) [6,18], micronucleation [17,19] and neoplastic transformations [11].…”

Section: Introductionmentioning

confidence: 99%

“…It was demonstrated by some investigators [24,25] that double strand breaks can be initiated by I-Sce1 at pre-determined location in a mammalian genome. It was also argued that non-nuclear targets in the cytoplasm can also produce bystander effects after irradiation [14,26].…”

Section: Introductionmentioning

confidence: 99%

Use of E18 Cell Model to Quantify DNA Strand Break Associated Bystander Effect (DSB-ABE)

Jalal¹

2017

J Carcinog Mutagen

View full text Add to dashboard Cite

Citation: Nasir J (2017) Use of E18 Cell Model to Quantify DNA Strand Break Associated Bystander Effect (DSB-ABE). J Carcinogene Mutagene 8: 295. doi: 10.4172/2157-2518.1000295 Copyright: © 2017 Nasir J. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. AbstractThe lymphoblast cell line E18 is a derivative of TK6 and has an I-Sce1 insert in the intron 2 of heterozygous TK1/ tk1 gene. E18 can be targeted with I-Sce1 restriction endonuclease to induce double strand breaks at the I-Sce1 site to measure radiation independent DNA damage and the associated bystander effect. For construction of E18 cell line an Eco47III site was inserted into the pTK-UAS linearized plasmid backbone and annealed with blunt-ended oligonucleotides of ISce1 restriction sequence in the presence of DNA ligase. DH5-α cells were transformed by heat transfecting the cells with pTK-UAS-Eco47III-Sce1 and selecting ampicillin resistant colonies. Plasmid DNA was extracted and analyzed for the presence of Eco47III and I-Sce1 sites. A clone with I-Sce site in intron 2 of the thymidine kinase active allele was selected for further experimentation and named E18. This model was tested to demonstrate the double strand break induced mutations and these strand breaks can also produce DNA strand break associated bystander effect (DSB-ABE) as measured by increased mutation frequency in naïve cells. The plasmid pAdTrackCMV I-Sce1 carrying GFP marker was electroporated in E18 cells to express the I-Sce1 restriction endonuclease which specifically targets the I-Sce1 site at intron 2 of the active TK allele. Mutation fraction assay was employed to measure direct mutation fraction (DMF) or accompanied by conditioned medium transfer to naïve cells for measuring bystander mutation fraction (BMF) as an end-point of targeting E18 with an exogenous I-Sce1 expression via pAdTrackCMV I-Sce1 to induce DNA damage and quantify DMF and BMF.

show abstract

What role for DNA damage and repair in the bystander response?

Cited by 42 publications

References 36 publications

Lack of Bystander Effects from High-LET Radiation for Early Cytogenetic End Points

Lack of Bystander Effects from High-LET Radiation for Early Cytogenetic End Points

γH2AX in Bystander Cells: Not Just a Radiation-Triggered Event, a Cellular Response to Stress Mediated by Intercellular Communication

Use of E18 Cell Model to Quantify DNA Strand Break Associated Bystander Effect (DSB-ABE)

Contact Info

Product

Resources

About