2021/04/22 更新

写真b

山本 久美子 (ヤマモト クミコ)

YAMAMOTO Kumiko

助教

出身大学院 【 表示 / 非表示

  • 2016年04月
    -
    2020年03月

    北海道大学  獣医学研究科  博士課程  修了

  • 2014年04月
    -
    2016年03月

    北海道教育大学  教育学研究科  教科教育専攻 理科教育専修  修士課程  修了

取得学位 【 表示 / 非表示

  • 北海道大学 -  博士(獣医学)

  • 北海道教育大学 -  修士(教育学)

学内職務経歴 【 表示 / 非表示

  • 2020年04月
    -
    継続中

    東京農業大学   生物産業学部   食香粧化学科   助教  

論文 【 表示 / 非表示

  • Using the larvae of caddisfly as a biomonitor to assess the spatial distribution and effective half-life of radiocesium in riverine environments in Fukushima, Japan

    Yuki Matsuo, Kunihiko Nakai, Nozomi Tatsuta, Osamu Inanami, Kumiko Yamamoto, Hazuki Mizukawa, Hiromitsu Nagasaka, Futoshi Mizutani, Youichi Chisaki, Toshiki Aiba, Takashi Ohba, Izumi Watanabe, Hiromi Nabeshi, Taiki Higuchi, Yuki Koga, Hideaki Matsumoto, Kou Nishimuta, Hideki Miyamoto, Tomokazu Haraguchi, Noriko Ryuda, Daisuke Ueno

    Physics Open ( Elsevier BV )  6   100060 - 100060   2021年02月  [査読有り]

    研究論文(学術雑誌)   共著

    DOI

  • Radiation-induced abnormal centrosome amplification and mitotic catastrophe in human cervical tumor HeLa cells and murine mammary tumor EMT6 cells

    Masaki Fujimoto, Tomoki Bo, Kumiko Yamamoto, Hironobu Yasui, Tohru Yamamori, Osamu Inanami

    Journal of Clinical Biochemistry and Nutrition ( The Society for Free Radical Research Japan )  67 ( 3 ) 240 - 247   2020年11月  [査読有り]

    研究論文(学術雑誌)   共著

    DOI

  • Mitochondrial fission promotes radiation-induced increase in intracellular Ca2+ level leading to mitotic catastrophe in mouse breast cancer EMT6 cells.

    Tomoki Bo, Tohru Yamamori, Kumiko Yamamoto, Masaki Fujimoto, Hironobu Yasui, Osamu Inanami

    Biochemical and biophysical research communications   522 ( 1 ) 144 - 150   2020年01月  [査読有り]

    研究論文(学術雑誌)   共著

    Mitochondrial dynamics are crucial for cellular survival in response to various stresses. Previously, we reported that Drp1 promoted mitochondrial fission after x-irradiation and its inhibition resulted in reduced cellular radiosensitivity and mitotic catastrophe. However, the mechanisms of radiation-induced mitotic catastrophe related to mitochondrial fission remain unclear. In this study, we investigated the involvement of cellular ATP production, ROS generation, and Ca2+ levels in mitotic catastrophe in EMT6 cells. Knockdown of Drp1 and Fis1, which are mitochondrial fission regulators, resulted in elongated mitochondria and significantly attenuated cellular radiosensitivity. Reduced mitochondrial fission mainly decreased mitotic catastrophe rather than necrosis and apoptosis after irradiation. Cellular ATP contents in Drp1 and Fis1 knockdown cells were similar to those in control cells. N-acetylcysteine and 2-glucopyranoside ascorbic acid have no effect on mitotic catastrophe after irradiation. The cellular [Ca2+]i level increased after irradiation, which was completely suppressed by Drp1 and Fis1 inhibition. Furthermore, BAPTA-AM significantly reduced radiation-induced mitotic catastrophe, indicating that cellular Ca2+ is a key mediator of mitotic catastrophe induction after irradiation. These results suggest that mitochondrial fission is associated with radiation-induced mitotic catastrophe via cytosolic Ca2+ regulation.

    DOI PubMed

  • Inhibition of ubiquitin-specific protease 2 causes accumulation of reactive oxygen species, mitochondria dysfunction, and intracellular ATP decrement in C2C12 myoblasts.

    Mayuko Hashimoto, Natsuko Saito, Haru Ohta, Kumiko Yamamoto, Asuka Tashiro, Kosuke Nakazawa, Osamu Inanami, Hiroshi Kitamura

    Physiological reports   7 ( 14 ) e14193   2019年07月  [査読有り]

    研究論文(学術雑誌)   共著

    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.

    DOI PubMed

  • In Vivo Extracellular pH Mapping of Tumors Using Electron Paramagnetic Resonance

    Denis A. Komarov, Yuki Ichikawa, Kumiko Yamamoto, Neil J. Stewart, Shingo Matsumoto, Hironobu Yasui, Igor A. Kirilyuk, Valery V. Khramtsov, Osamu Inanami, Hiroshi Hirata

    ANALYTICAL CHEMISTRY ( AMER CHEMICAL SOC )  90 ( 23 ) 13938 - 13945   2018年12月  [査読有り]

    研究論文(学術雑誌)   共著

    An electron paramagnetic resonance (EPR)based method for noninvasive three-dimensional extracellular pH mapping was developed using a pH-sensitive nitroxyl radical as an exogenous paramagnetic probe. Fast projection scanning with a constant magnetic field sweep enabled the acquisition of four-dimensional (3D spatial +1D spectral) EPR images within 7.5 min. Three-dimensional maps of pH were reconstructed by processing the pH-dependent spectral information on the images. To demonstrate the proposed method of pH mapping, the progress of extracellular acidosis in tumor-bearing mouse legs was studied. Furthermore, extracellular pH mapping was used to visualize the spatial distribution of acidification in different tumor xenograft mouse models of human-derived pancreatic ductal adenocarcinoma cells. The proposed EPR-based pH mapping method enabled quantitative visualization of regional changes in extracellular pH associated with altered tumor metabolism.

    DOI PubMed

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