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Adaptive response in embryogenesis: Comparative microarray analysis of gene expressions in mouse fetuses
https://repo.qst.go.jp/records/61794
https://repo.qst.go.jp/records/61794dd688686-52b4-4f73-842d-94dcb3353b5c
Item type | 会議発表用資料 / Presentation(1) | |||||
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公開日 | 2006-09-20 | |||||
タイトル | ||||||
タイトル | Adaptive response in embryogenesis: Comparative microarray analysis of gene expressions in mouse fetuses | |||||
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× Shang, Yi× Ohyama, Harumi× Tanaka, Kaoru× Nakajima, Tetsuo× Nenoi, Mitsuru× Hayata, Isamu× Guillaume Vares× 王 冰× 尚 奕× 大山 ハルミ× 田中 薫× 中島 徹夫× 根井 充× 早田 勇 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Exposure of sublethal doses of ionizing radiation can induce protective mechanisms against a subsequent higher dose irradiation. This phenomenon, called radiation-induced adaptive response (AR), has been described in a wide range of biological models. We previously demonstrated the existence of AR in mice during late organogenesis. For better understanding of molecular mechanisms underlying AR in this model, we performed a global analysis of transcriptome regulations in cells collected from whole mouse fetuses, after in utero exposure to priming irradiation. Several combinations of radiation dose and dose-rate were applied to induce or not an AR in our system. While many genes were not modulated at all after radiation exposure and several genes were deregulated for all conditions, we identified a panel of genes (so called AR genes) showing significantly different expression ratios in AR and non AR-inducing conditions. Since AR genes were implicated in a variety of functions and cellular processes, we applied a functional classification algorithm which clustered genes in a limited number of functionally related groups. We also established that AR genes are significantly enriched for specific keywords. Our results suggested the involvement of signal transduction and p53-related pathways in the induction of AR, as well as possible consequences for subsequent developmental process. Even though no evidence of specific DNA repair modulation at the transcriptional level was observed in adapted cells, we studied H2AX phosphorylation kinetics following challenging irradiation in adapted and non-adapted fetal liver cells and observed that H2AX phosphorylation peak appeared earlier in adapted than in non adapted cells (while disappearance rates were similar), which could indeed suggest a possible modulation of DNA repair induced by priming radiation exposure. However, no modulation of radiation-induced cell death by AR was described in fetal liver cells. Taken together, our results present the first evidence of molecular mechanisms modulation by AR in utero, which may have potentially important consequences for further developmental processes, and could even influence tumorigenesis. The late effects occurring in mice adapted in utero, such as chromosomal aberrations or cancer initiation) therefore are a promising and interesting area for future research. | |||||
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 | New Nuclear Research Symposium on Biological Response to Low Dose Radiation- New Aspects of Low Dose Radiation Effects | |||||
発表年月日 | ||||||
日付 | 2006-09-08 | |||||
日付タイプ | Issued |