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Inhibition of ubiquitin‐specific protease 2 causes accumulation of reactive oxygen species, mitochondria dysfunction, and intracellular ATP decrement in C2C12 myoblasts
http://hdl.handle.net/10659/00006640
http://hdl.handle.net/10659/00006640c86abb1f-a395-4887-a9e0-68ecb669b82b
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
R-2020-75_kitamura.pdf (1.1 MB)
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| Item type | 学術雑誌論文 / Journal Article(1) | |||||
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| 公開日 | 2020-11-18 | |||||
| タイトル | ||||||
| タイトル | Inhibition of ubiquitin‐specific protease 2 causes accumulation of reactive oxygen species, mitochondria dysfunction, and intracellular ATP decrement in C2C12 myoblasts | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | USP | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | myoblast | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | mitochondria | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | respiratory chain | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | oxidative phosphorylation | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | USP | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | myoblast | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | mitochondria | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | respiratory chain | |||||
| キーワード | ||||||
| 言語 | en | |||||
| 主題Scheme | Other | |||||
| 主題 | oxidative phosphorylation | |||||
| 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 | |||||
| 著者 |
Hashimoto, Mayuko
× Hashimoto, Mayuko× Saito, Natsuko× Ohta, Haru× Yamamoto, Kumiko× Tashiro, Asuka× Nakazawa, Kosuke× Inanami, Osamu× 北村, 浩 |
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| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | Ubiquitin‐specific protease 2 (USP2) is considered to participate in the differentiation of myoblasts to myotubes, however, its functions in myoblasts under growth conditions remain elusive. In this study, we analyzed the physiological roles of USP2 in myoblasts using Usp2 knockout (KO) C2C12 cells as well as a USP2 specific inhibitor. In addition to the disruption of differentiation, clustered regularly interspaced short palindromic repeats/Cas9‐generated Usp2KO cells exhibited inhibition of proliferation compared to parental C2C12 cells. Usp2KO cells reduced the accumulation of intracellular adenosine triphosphate (ATP) content and oxygen consumption. Moreover, Usp2KO cells had fragmented mitochondria, suggesting that mitochondrial respiration was inactive. The deficiency of Usp2 did not affect the enzymatic activities of respiratory chain complexes I, III, IV, and V. However, mitochondrial membrane permeability—evaluated using calcein AM‐cobalt staining—was increased in Usp2KO cells. The membrane potential of Usp2KO cells was clearly decreased. Usp2KO cells accumulated reactive oxygen species (ROS) in the mitochondria. The USP2‐selective inhibitor ML364 also increased the levels of mitochondrial ROS, and modulated the membrane potential and morphology of the mitochondria. These effects were followed by a decrement in the intracellular content of ATP. Based on these findings, we speculate that USP2 may be involved in maintaining the integrity of the mitochondrial membrane. This process ensures the supply of ATP in myoblasts, presumably leading to proliferation and differentiation. | |||||
| 書誌情報 |
Physiological Reports 巻 7, 号 14, p. e14193-1-e14193-14, 発行日 2019-07 |
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| ISBN | ||||||
| 識別子タイプ | ISBN | |||||
| 関連識別子 | 2051-817X | |||||
| DOI | ||||||
| 関連タイプ | isIdenticalTo | |||||
| 識別子タイプ | DOI | |||||
| 関連識別子 | https://doi.org/10.14814/phy2.14193 | |||||
| 権利（URI） | ||||||
| 権利情報 | http://creativecommons.org/licenses/by/4.0/ | http://creativecommons.org/licenses/by/4.0/ | |||||
| 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 | |||||
| 出版者 | ||||||
| 出版者 | John Wiley & Sons, Inc. | |||||
| 資源タイプ | ||||||
| 内容記述タイプ | Other | |||||
| 内容記述 | Article | |||||
