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    The involvement of calcium and MAP kinase signaling pathways in the production of radiation-induced bystander effects.

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    Authors
    Lyng, F M
    Maguire, P
    McClean, B
    Seymour, C
    Mothersill, C
    Issue Date
    2006-04
    Keywords
    BYSTANDER EFFECTS
    RADIATION
    NEOPLASMS
    MeSH
    Bystander Effect
    Calcium
    Calcium Signaling
    Cell Line
    Dose-Response Relationship, Radiation
    Humans
    Keratinocytes
    MAP Kinase Signaling System
    Mitogen-Activated Protein Kinases
    Radiation Dosage
    Signal Transduction
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    Citation
    The involvement of calcium and MAP kinase signaling pathways in the production of radiation-induced bystander effects. 2006, 165 (4):400-9 Radiat. Res.
    Journal
    Radiation research
    URI
    http://hdl.handle.net/10147/621399
    PubMed ID
    16579652
    Abstract
    Much evidence now exists regarding radiation-induced bystander effects, but the mechanisms involved in the transduction of the signal are still unclear. The mitogen-activated protein kinase (MAPK) pathways have been linked to growth factor-mediated regulation of cellular events such as proliferation, senescence, differentiation and apoptosis. Activation of multiple MAPK pathways such as the ERK, JNK and p38 pathways have been shown to occur after exposure of cells to radiation and a variety of other toxic stresses. Previous studies have shown oxidative stress and calcium signaling to be important in radiation-induced bystander effects. The aim of the present study was to investigate MAPK signaling pathways in bystander cells exposed to irradiated cell conditioned medium (ICCM) and the role of oxidative metabolism and calcium signaling in the induction of bystander responses. Human keratinocytes (HPV-G cell line) were irradiated (0.005-5 Gy) using a cobalt-60 teletherapy unit. The medium was harvested 1 h postirradiation and transferred to recipient HPV-G cells. Phosphorylated forms of p38, JNK and ERK were studied by immunofluorescence 30 min-24 h after exposure to ICCM. Inhibitors of the ERK pathway (PD98059 and U0126), the JNK pathway (SP600125), and the p38 pathway (SB203580) were used to investigate whether bystander-induced cell death could be blocked. Cells were also incubated with ICCM in the presence of superoxide dismutase, catalase, EGTA, verapamil, nifedipine and thapsigargin to investigate whether bystander effects could be inhibited because of the known effects on calcium homeostasis. Activated forms of JNK and ERK proteins were observed after exposure to ICCM. Inhibition of the ERK pathway appeared to increase bystander-induced apoptosis, while inhibition of the JNK pathway appeared to decrease apoptosis. In addition, reactive oxygen species, such as superoxide and hydrogen peroxide, and calcium signaling were found to be important modulators of bystander responses. Further investigations of these signaling pathways may aid in the identification of novel therapeutic targets.
    Item Type
    Article
    Language
    en
    ISSN
    0033-7587
    Collections
    St. Luke's Radiation Oncology Network, Dublin

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