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DNA damage-induced apoptosis in C3H mouse peritoneal resident macrophages
https://repo.qst.go.jp/records/69017
https://repo.qst.go.jp/records/69017b658d18d-6948-4802-a604-862813325287
| Item type | 会議発表用資料 / Presentation(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2007-07-17 | |||||
| タイトル | ||||||
| タイトル | DNA damage-induced apoptosis in C3H mouse peritoneal resident macrophages | |||||
| 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 |
Kubota, Yoshihisa
× Kubota, Yoshihisa× Suetomi, Katsutoshi× Fujimori, Akira× Takahashi, Sentaro× 久保田 善久× 末冨 勝敏× 藤森 亮× 高橋 千太郎 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Previously we reported irradiation-induced apoptosis in peritoneal resident macrophages (PRM) of C3H mice but not other strains of mice. Studies with atm knockout, p53 knockout or scid mice suggested that a well-known DNA damage-induced apoptotic pathway involving the activation of ATM, DNA-PK and/or TP53 did not take part in irradiation-induced apoptosis in C3H mouse PRM. Furthermore, superoxide anion and the depletion of Mcl-1, an anti-apoptotic Bcl-2 family protein, through irradiation-induced arrest of global protein synthesis were identified as critical factors for the apoptosis. The present study was planed to reconfirm the involvement of reactive oxygen species but not DNA damage in irradiation-induced apoptosis in C3H mouse PRM. PRM were treated with paraquat (a superoxide inducer), hydrogen peroxide or cadmium at various concentrations to enhance intracellular level of reactive oxygen species or oxidative stress. As a selective indicator of irradiation-induced apoptosis in C3H mouse PRM, Mcl-1 level was examined by western blotting. Hydrogen peroxide and cadmium treatment did not affect the amount of Mcl-1. Paraquat slightly diminished Mcl-1 at extremely high concentrations where oxidative stress was elicited as severely as caspase 3 was completely inactivated. On the other hand, Mcl-1 was markedly depleted by gamma-irradiation or UV irradiation in C3H mouse PRM. PRM were treated with DNA topoisomerase II inhibitor, etoposide or introduced with a restriction endonuclease, Pvu II by means of HVJ envelope vector kit (GenomeONETM) to generate DNA double-strand breaks. Unexpectedly, these treatments induced marked apoptosis in C3H mouse PRM, but not in radioresistant B6 mouse PRM. Therefore, it is concluded that irradiation-induced apoptosis in C3H mouse PRM is attributable to irradiation-induced DNA damage, possibly DNA double-strand breaks. | |||||
| 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 | International Congress of Radiation Research | |||||
| 発表年月日 | ||||||
| 日付 | 2007-07-12 | |||||
| 日付タイプ | Issued | |||||
