WEKO3
アイテム
Nuclear factor (erythroid-derived 2)-like 2 antioxidative response mitigates cytoplasmic radiation-induced DNA double-strand breaks
https://repo.qst.go.jp/records/49536
https://repo.qst.go.jp/records/4953676d8ecc7-f2ff-4df8-b161-39f233050eb8
| Item type | 学術雑誌論文 / Journal Article(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2018-12-03 | |||||
| タイトル | ||||||
| タイトル | Nuclear factor (erythroid-derived 2)-like 2 antioxidative response mitigates cytoplasmic radiation-induced DNA double-strand breaks | |||||
| 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_6501 | |||||
| 資源タイプ | journal article | |||||
| 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 |
Wang, Jun
× Wang, Jun× Konishi, Teruaki× Konishi, Teruaki |
|||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | It has been reported that DNA double-strand breaks (DSB) can be induced by cytoplasm irradiation, and that both reactive free radicals and mitochondria are involved in DSB formation. However, the cellular antioxidative responses that are stimulated and the biological consequences of cytoplasmic irradiation remain unknown. Using the Single Particle Irradiation System to Cells proton microbeam facility at the National Institute of Radiological Sciences (Japan), the response of nuclear factor (erythroid-derived 2)-like 2 (NRF2) antioxidative signaling to cytoplasmic irradiation was studied in normal human lung fibroblast WI-38 cells. Cytoplasmic irradiation stimulated the localization of NRF2 to the nucleus and the expression of its target protein, heme oxygenase 1. Activation of NRF2 by tert-Butylhydroquinone mitigated the levels of DSB induced by cytoplasmic irradiation. Mitochondrial fragmentation was also promoted by cytoplasmic irradiation, and treatment with the mitochondrial fragmentation inhibitor Mdivi-1 suppressed cytoplasmic irradiation-induced NRF2 activation and aggravated DSB formation. Furthermore, p53 contributed to the induction of mitochondrial fragmentation and activation of NRF2, although the expression of p53 was significantly downregulated by cytoplasmic irradiation. Finally, mitochondrial superoxide (MitoSOX) production was enhanced under cytoplasmic irradiation, and the usage of the MitoSOX scavenger mito-tempol indicated that MitoSOX elicited alterations in p53 expression, mitochondrial dynamics, and NRF2 activation. Overall, NRF2 antioxidative response is suggested to play a key role against genomic DNA damage under cytoplasmic irradiation. Additionally, the upstream regulators of NRF2 provide new clues on cytoplasmic irradiation-induced biological processes and prevention of radiation risks. | |||||
| 書誌情報 |
Cancer Science 巻 110, p. 686-696, 発行日 2018-12 |
|||||
| 出版者 | ||||||
| 出版者 | John Wiley & Sons, Inc. | |||||
| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 1349-7006 | |||||
| PubMed番号 | ||||||
| 識別子タイプ | PMID | |||||
| 関連識別子 | 30561156 | |||||
| DOI | ||||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | 10.1111/cas.13916 | |||||
| 関連サイト | ||||||
| 識別子タイプ | URI | |||||
| 関連識別子 | https://onlinelibrary.wiley.com/doi/abs/10.1111/cas.13916 | |||||
