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Further, we observed that aquaporin (AQP) 3, 5, and 8 bind nicotinamide-adenine dinucleotide phosphate oxidase 2 and regulate the permeability of extracellular H2O2, thereby contributing to ferroptosis. Additionally, the role of mitochondria in ferroptosis was investigated using mitochondrial transfer in ρ0 cells. When mitochondria were transferred into ρ0 cells, the cells exhibited no sensitivity to H2O2-induced cytotoxicity because of decreased Fe2+ levels. Moreover, mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQP expression. Our findings also revealed the involvement of AQP and PHB2 in ferroptosis. 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Mitochondrial dysfunction promotes aquaporin expression that controls hydrogen peroxide permeability and ferroptosis
http://hdl.handle.net/10232/00031697
http://hdl.handle.net/10232/000316976a14afef-568b-4308-8ffc-b86b41352c30
名前 / ファイル | ライセンス | アクション |
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Item type | 学位論文 / Thesis or Dissertation(1) | |||||
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公開日 | 2021-04-09 | |||||
タイトル | ||||||
タイトル | Mitochondrial dysfunction promotes aquaporin expression that controls hydrogen peroxide permeability and ferroptosis | |||||
別言語のタイトル | ||||||
その他のタイトル | ミトコンドリア機能障害は過酸化水素の膜透過性とフェロトーシスを制御するアクアポリンの発現を促進させる | |||||
著者 |
高, 裕子
× 高, 裕子 |
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著者よみ | ||||||
姓名 | タカシ, ユウコ | |||||
別言語の著者 | ||||||
姓名 | TAKASHI, Yuko | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題言語 | en | |||||
主題Scheme | Other | |||||
主題 | Mitochondria | |||||
キーワード | ||||||
主題言語 | en | |||||
主題Scheme | Other | |||||
主題 | Ferroptosis | |||||
キーワード | ||||||
主題言語 | en | |||||
主題Scheme | Other | |||||
主題 | Aquaporin | |||||
キーワード | ||||||
主題言語 | en | |||||
主題Scheme | Other | |||||
主題 | Hydrogen peroxide | |||||
キーワード | ||||||
主題言語 | en | |||||
主題Scheme | Other | |||||
主題 | Fe2+ | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_db06 | |||||
資源タイプ | doctoral thesis | |||||
アクセス権 | ||||||
アクセス権 | open access | |||||
アクセス権URI | http://purl.org/coar/access_right/c_abf2 | |||||
要約(Abstract) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Most anti-cancer agents and radiotherapy exert their therapeutic effects via the production of free radicals. Ferroptosis is a recently described cell death process that is accompanied by iron-dependent lipid peroxidation. Hydrogen peroxide (H2O2) has been reported to induce cell death. However, it remains controversial whether H2O2-induced cell death is ferroptosis. In the present study, we aimed to elucidate the involvement of mitochondria in H2O2-induced ferroptosis and examined the molecules that regulate ferroptosis. We found that one mechanism underlying H2O2-induced cell death is ferroptosis, which occurs soon after H2O2 treatment (within 3 h after H2O2 treatment). We also investigated the involvement of mitochondria in H2O2-induced ferroptosis using mitochondrial DNA-depleted ρ0 cells because ρ0 cells produce more lipid peroxidation, hydroxyl radicals (•OH), and are more sensitive to H2O2 treatment. We found that ρ0 cells contain high Fe2+ levels that lead to •OH production by H2O2. Further, we observed that aquaporin (AQP) 3, 5, and 8 bind nicotinamide-adenine dinucleotide phosphate oxidase 2 and regulate the permeability of extracellular H2O2, thereby contributing to ferroptosis. Additionally, the role of mitochondria in ferroptosis was investigated using mitochondrial transfer in ρ0 cells. When mitochondria were transferred into ρ0 cells, the cells exhibited no sensitivity to H2O2-induced cytotoxicity because of decreased Fe2+ levels. Moreover, mitochondrial transfer upregulated the mitochondrial quality control protein prohibitin 2 (PHB2), which contributes to reduced AQP expression. Our findings also revealed the involvement of AQP and PHB2 in ferroptosis. Our results indicate that H2O2 treatment enhances AQP expression, Fe2+ level, and lipid peroxidation, and decrease mitochondrial function by downregulating PHB2, and thus, is a promising modality for effective cancer treatment. | |||||
要約(Abstract) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Yuko Takashi, Kazuo Tomita, Yoshikazu Kuwahara, Mehryar Habibi Roudkenar, Amaneh Mohammadi Roushandeh, Kento Igarashi Taisuke Nagasawa, Yoshihiro Nishitani, Tomoaki Sato Mitochondrial dysfunction promotes aquaporin expression that controls hydrogen peroxide permeability and ferroptosis Free Radical Biology and Medicine 161, 2020, p.60-70 https://doi.org/10.1016/j.freeradbiomed.2020.09.027 |
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作成日 | ||||||
日付 | 2021-02-09 | |||||
出版タイプ | ||||||
出版タイプ | VoR | |||||
出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
NDC | ||||||
主題Scheme | NDC | |||||
主題 | 490 | |||||
ファイル(説明) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 博士論文全文 | |||||
ファイル(説明) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 博士論文要旨 | |||||
ファイル(説明) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 最終試験結果の要旨 | |||||
ファイル(説明) | ||||||
内容記述タイプ | Other | |||||
内容記述 | 論文審査の要旨 | |||||
公開者・出版者 | ||||||
出版者 | 鹿児島大学 | |||||
公開者・出版者 | ||||||
出版者 | Elsevier | |||||
公開者よみ | ||||||
公開者よみ | カゴシマ ダイガク | |||||
公開者別名 | ||||||
公開者別名 | Kagoshima University | |||||
備考 | ||||||
備考 | 【指導教員:西谷佳浩】 | |||||
date.appl | ||||||
【学位申請日】2020-12-02 | ||||||
学位名 | ||||||
学位名 | 博士(歯学)Doctor of Philosophy in Dental Science | |||||
学位授与機関 | ||||||
学位授与機関識別子Scheme | kakenhi | |||||
学位授与機関識別子 | 17701 | |||||
学位授与機関名 | 鹿児島大学 | |||||
学位授与年月日 | ||||||
学位授与年月日 | 2021-02-25 | |||||
学位授与番号 | ||||||
学位授与番号 | 甲総研第582号 |