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Several of our\nAR experimental models will be introduced in this presentation.\nWe demonstrated the existence of AR in mice during late organogenesis.\nMolecular mechanisms underlying AR in this model were investigated. Using\nDNA microarrays and real-time quantitative fluorescence RT-PCR, AR-specific\ngene modulations were identified. Our results suggested the involvement of\nsignal transduction and p53-related pathways in the induction of AR, in\nagreement with previous investigations showing that AR could be dependent on\np53 activity. The observed gene modulations may also have possible\nconsequences for subsequent developmental process of the fetus. This is the\nfirst report of AR-specific modulations at the molecular level in utero,\nwhich could serve as a basis for subsequent studies aimed at understanding\nAR in this model and possible long term effects. In addition, analysis of\np53 protein levels in adapted murine fetal limb bud cells cultured in vitro\nwill be presented and the involvement of p53 in AR will be discussed.\nWe also focused our interest on the possibility of observing an AR when\nusing high-LET radiation. Knowing that high-LET heavy-ion radiations\nproduce non-randomly distributed DNA damage in the form of clusters, or\nlocally multiply damaged sites (LMDS), we tried to investigate whether this\nkind of damage can trigger an AR specific DNA repair, and whether AR\ncould protect against LMDS induction by challenging radiations. Biological\neffects of low and high-LET irradiation (performed at HIMAC, Chiba) were\nstudied in vitro in cultured lymphoblastoid cell lines, which were exposed\nto priming and/or challenging radiation (either X-Rays or accelerated\nheavy-ions at various LETs). Our results demonstrated the existence of a\nmutagenic AR in this model, and pointed to a possible involvement of DSB\nrepair mechanisms. The ability of high LET heavy-ion radiation (at low dose\nand low dose-rate) to induce AR is under investigation. 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Radiation-induced Adaptive Response: in vitro and in utero Studies
https://repo.qst.go.jp/records/62944
https://repo.qst.go.jp/records/6294427da98b4-b40f-4530-9b10-3886df6ceae7
Item type | 会議発表用資料 / Presentation(1) | |||||
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公開日 | 2009-01-09 | |||||
タイトル | ||||||
タイトル | Radiation-induced Adaptive Response: in vitro and in utero Studies | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_c94f | |||||
資源タイプ | conference object | |||||
アクセス権 | ||||||
アクセス権 | metadata only access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_14cb | |||||
著者 |
Vares, Guillaume
× Vares, Guillaume× Bing, Wang× Tanaka, Kaoru× Shang, Yi× Murakami, Masahiro× KAKIMOTO, AYANA× Eguchi-Kasai, Kiyomi× Nakajima, Tetsuo× Ohyama, Harumi× Hayata, Isamu× Nenoi, Mitsuru× Guillaume Vares× 王 冰× 田中 薫× 尚 奕× 村上 正弘× 柿本 彩七× 笠井 清美× 中島 徹夫× 大山 ハルミ× 早田 勇× 根井 充 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | In contradiction to classical paradigm, which assumes that radiation effects are directly proportional to energy deposit, numerous in vitro, in vivo and in utero studies, including ours, described the existence in various models of a radiation-induced adaptive response (AR), according to which pre-exposure to low priming dose of ionizing radiations decreases the biological effects of a subsequent higher challenging dose. Several of our AR experimental models will be introduced in this presentation. We demonstrated the existence of AR in mice during late organogenesis. Molecular mechanisms underlying AR in this model were investigated. Using DNA microarrays and real-time quantitative fluorescence RT-PCR, AR-specific gene modulations were identified. Our results suggested the involvement of signal transduction and p53-related pathways in the induction of AR, in agreement with previous investigations showing that AR could be dependent on p53 activity. The observed gene modulations may also have possible consequences for subsequent developmental process of the fetus. This is the first report of AR-specific modulations at the molecular level in utero, which could serve as a basis for subsequent studies aimed at understanding AR in this model and possible long term effects. In addition, analysis of p53 protein levels in adapted murine fetal limb bud cells cultured in vitro will be presented and the involvement of p53 in AR will be discussed. We also focused our interest on the possibility of observing an AR when using high-LET radiation. Knowing that high-LET heavy-ion radiations produce non-randomly distributed DNA damage in the form of clusters, or locally multiply damaged sites (LMDS), we tried to investigate whether this kind of damage can trigger an AR specific DNA repair, and whether AR could protect against LMDS induction by challenging radiations. Biological effects of low and high-LET irradiation (performed at HIMAC, Chiba) were studied in vitro in cultured lymphoblastoid cell lines, which were exposed to priming and/or challenging radiation (either X-Rays or accelerated heavy-ions at various LETs). Our results demonstrated the existence of a mutagenic AR in this model, and pointed to a possible involvement of DSB repair mechanisms. The ability of high LET heavy-ion radiation (at low dose and low dose-rate) to induce AR is under investigation. Some perspectives for this study will also be discussed. |
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会議概要(会議名, 開催地, 会期, 主催者等) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 第3回放射線防護研究センターシンポジウム | |||||
発表年月日 | ||||||
日付 | 2008-12-16 | |||||
日付タイプ | Issued |