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Over-activation of cAMP signaling increases vulnerability to hydrogen peroxide via actin rearrangement, which is inhibited by prostaglandin E2 in a mouse granulosa cell line.
https://tmdu.repo.nii.ac.jp/records/174
https://tmdu.repo.nii.ac.jp/records/174afe638eb-8fb2-4c6b-a334-a289c0128528
名前 / ファイル | ライセンス | アクション |
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01_koushi (988.4 kB)
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Copyright © 2007 Tokyo Medical and Dental University (TMDU)
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Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
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公開日 | 2017-08-10 | |||||
タイトル | ||||||
タイトル | ||||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | granulosa cells | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | oxidative stress | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | cAMP | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | prostaglandin E2 | |||||
キーワード | ||||||
主題Scheme | Other | |||||
主題 | actin | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | granulosa cells | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | oxidative stress | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | cAMP | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | prostaglandin E2 | |||||
キーワード | ||||||
言語 | en | |||||
主題Scheme | Other | |||||
主題 | actin | |||||
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 | departmental bulletin paper | |||||
著者 |
Koushi, Masami
× Koushi, Masami× 亀井, 美子× 青山, 靖典× 朝海, 怜× 滝澤, 登一郞 |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Apoptosis of granulosa cells (GC) contributes to ovarian follicular atresia, and has been implicated to depend on the oxidant status of GC within follicles. Here, we investigated the effects of cAMP and prostaglandin E2 (PGE2) on sensitivity to oxidative stress using 4B2 cells with cAMP-dependent, steroidogenic and differentiated properties. This cell line was isolated from mouse GC co-transfected with genes for SV40 large T antigen and Ad4BP/SF1 transcription factor (Kamei et al. 2005). Treatment of serum-starved cells with 8-Br-cAMPcaused 30 to 40% of the cells to become polygonal within 2 h through actin rearrangement. Interestingly, H2O2 treatment showed that these polygonal cells were vulnerable to oxidative stress that led to cell death, which was inhibited by pretreatment with phalloidin, an F-actin stabilizing agent. Although PGE2 alone had no effect, cotreatment with PGE2 and 8-Br-cAMP completely inhibited the effects of 8-Br-cAMP on cell shape change and oxidative stress vulnerability through phosphatidylinositol 3-kinase (PI3K)-dependent manner. Notably, PGE2 and 8-Br-cAMP cooperated additively to increase progesterone secretion. These data suggest that cAMP signaling in GC may enhance oxidative stress risk through actin rearrangement, and PGE2 may reduce such risk through activating PI3K, while cooperating with cAMP signaling in steroidogenesis. | |||||
書誌情報 |
Journal of Medical and Dental Sciences en : Journal of Medical and Dental Sciences 巻 54, 号 4, p. 167-176, 発行日 2007-12 |
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出版者 | ||||||
出版者 | 国立大学法人 東京医科歯科大学 | |||||
ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 2185-9132 | |||||
書誌レコードID | ||||||
収録物識別子タイプ | NCID | |||||
収録物識別子 | AA12028964 | |||||
論文ID(NAID) | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | NAID | |||||
関連識別子 | 130005430206 | |||||
DOI | ||||||
関連タイプ | isIdenticalTo | |||||
識別子タイプ | DOI | |||||
関連識別子 | 10.11480/jmds.540401 | |||||
著者版フラグ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 |