2021/06/14 更新

写真a

サトウ マミ
佐藤 茉美
SATO Mami
所属
日本酒学センター 特任助教
職名
特任助教
外部リンク

学位

  • 博士(保健学) ( 2019年3月   新潟大学 )

  • 農学 ( 2016年3月   山形大学 )

  • 農学 ( 2014年3月   岩手大学 )

研究キーワード

  • アミノ酸輸送系

  • フェロトーシス

  • グルタチオン

  • 酸化ストレス

研究分野

  • ライフサイエンス / 細胞生物学  / アミノ酸トランスポーター

経歴(researchmap)

  • 新潟大学   日本酒学センター   特任助教

    2020年7月 - 現在

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  • ヘルムホルツセンターミュンヘン   Institute of Metabolism and Cell Death   博士研究員

    2019年5月 - 2020年5月

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    国名:ドイツ連邦共和国

    備考:公益財団法人 上原記念生命科学財団 ポストドクトラルフェローシップの助成を受けての留学

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  • 新潟大学   大学院保健学研究科   研究生

    2019年4月

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  • ヘルムホルツセンターミュンヘン   Institute of Developmental Genetics   文部科学省「トビタテ!留学JAPAN日本代表プログラム」第7期派遣留学生

    2017年10月 - 2018年7月

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    国名:ドイツ連邦共和国

    備考:文部科学省「トビタテ!留学JAPAN日本代表プログラム」の支援による留学

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経歴

  • 新潟大学   日本酒学センター   特任助教

    2020年7月 - 現在

学歴

  • 新潟大学   大学院保健学研究科   検査技術科学専攻

    2016年4月 - 2019年3月

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  • 山形大学   大学院農学研究科(修士課程)

    2014年4月 - 2016年3月

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  • 岩手大学   農学部   動物科学課程

    2010年4月 - 2014年3月

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所属学協会

  • 日本分子生物学会

    2020年11月 - 現在

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  • レドックスR&D戦略委員会

    2020年8月

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  • 日本生化学会

    2016年7月 - 現在

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留学歴

  • 2019年05月08日 - 2020年05月05日   ヘルムホルツセンター ミュンヘン   上原記念生命科学財団 ポストドクトラルフェローシップ

  • 2017年10月05日 - 2018年07月03日   ヘルムホルツセンター ミュンヘン   日本学生支援機構「官民協働海外留学支援制度 (トビタテ!留学JAPAN日本代表プログラム)」 派遣留学生

取得資格

  • 遺伝子分析科学認定士(初級)

 

論文

  • Diversity and distribution of ticks in Niigata prefecture, Japan (2016–2018): Changes since 1950 査読

    Megumi Sato, Sumire Ikeda, Reiko Arai, Miwako Kato, Junko Aoki, Akiko Nishida, Kaori Watanabe, Chika Hirokawa, Kozo Watanabe, Maria Angenica F. Regilme, Mami Sato, Marcello Otake Sato, Tsutomu Tamura

    Ticks and Tick-borne Diseases12 ( 3 ) 101683 - 101683   2021年5月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Elsevier BV  

    DOI: 10.1016/j.ttbdis.2021.101683

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  • Loss of the cystine/glutamate antiporter in melanoma abrogates tumor metastasis and markedly increases survival rates of mice 査読

    Mami Sato, Kunishige Onuma, Mio Domon, Shun Hasegawa, Ami Suzuki, Ryosuke Kusumi, Remi Hino, Nahoko Kakihara, Yusuke Kanda, Mitsuhiko Osaki, Junichi Hamada, Shiro Bannai, Regina Feederle, Katalin Buday, José Pedro Friedmann Angeli, Bettina Proneth, Marcus Conrad, Futoshi Okada, Hideyo Sato

    International Journal of Cancer   2020年8月

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    担当区分:筆頭著者   掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    DOI: 10.1002/ijc.33262

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    その他リンク: https://onlinelibrary.wiley.com/doi/full-xml/10.1002/ijc.33262

  • Inorganic polyphosphate potentiates lipopolysaccharide-induced macrophage inflammatory response. 査読 国際誌

    Toru Ito, Suguru Yamamoto, Keiichi Yamaguchi, Mami Sato, Yoshikatsu Kaneko, Shin Goto, Yuji Goto, Ichiei Narita

    The Journal of biological chemistry295 ( 12 ) 4014 - 4023   2020年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:American Society for Biochemistry & Molecular Biology (ASBMB)  

    Inorganic polyphosphate (polyP) is a linear polymer of orthophosphate units that are linked by phosphoanhydride bonds and is involved in various pathophysiological processes. However, the role of polyP in immune cell dysfunction is not well-understood. In this study, using several biochemical and cell biology approaches, including cytokine assays, immunofluorescence microscopy, receptor-binding assays with quartz crystal microbalance, and dynamic light scanning, we investigated the effect of polyP on in vitro lipopolysaccharide (LPS)-induced macrophage inflammatory response. PolyP up-regulated LPS-induced production of the inflammatory cytokines, such as tumor necrosis factor α, interleukin-1β, and interleukin-6, in macrophages, and the effect was polyP dose- and chain length-dependent. However, orthophosphate did not exhibit this effect. PolyP enhanced the LPS-induced intracellular macrophage inflammatory signals. Affinity analysis revealed that polyP interacts with LPS, inducing formation of small micelles, and the polyP-LPS complex enhanced the binding affinity of LPS to Toll-like receptor 4 (TLR4) on macrophages. These results suggest that inorganic polyP plays a critical role in promoting inflammatory response by enhancing the interaction between LPS and TLR4 in macrophages.

    DOI: 10.1074/jbc.RA119.011763

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  • FSP1 is a glutathione-independent ferroptosis suppressor 査読

    Sebastian Doll, Florencio Porto Freitas, Ron Shah, Maceler Aldrovandi, Milene Costa da Silva, Irina Ingold, Andrea Goya Grocin, Thamara Nishida Xavier da Silva, Elena Panzilius, Christina H. Scheel, André Mourão, Katalin Buday, Mami Sato, Jonas Wanninger, Thibaut Vignane, Vaishnavi Mohana, Markus Rehberg, Andrew Flatley, Aloys Schepers, Andreas Kurz, Daniel White, Markus Sauer, Michael Sattler, Edward William Tate, Werner Schmitz, Almut Schulze, Valerie O’Donnell, Bettina Proneth, Grzegorz M. Popowicz, Derek A. Pratt, José Pedro Friedmann Angeli, Marcus Conrad

    Nature575 ( 7784 ) 693 - 698   2019年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science and Business Media LLC  

    DOI: 10.1038/s41586-019-1707-0

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    その他リンク: http://www.nature.com/articles/s41586-019-1707-0

  • Adsorption of Protein-Bound Uremic Toxins Using Activated Carbon through Direct Hemoperfusion in vitro 査読

    Suguru Yamamoto, Toru Ito, Mami Sato, Shin Goto, Junichiro J. Kazama, Fumitake Gejyo, Ichiei Narita

    Blood Purification48 ( 3 ) 215 - 222   2019年

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:S. Karger AG  

    DOI: 10.1159/000500014

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  • The ferroptosis inducer erastin irreversibly inhibits system xc- and synergizes with cisplatin to increase cisplatin's cytotoxicity in cancer cells 査読

    Mami Sato, Ryosuke Kusumi, Shinji Hamashima, Sho Kobayashi, Satoru Sasaki, Yuhei Komiyama, Takuji Izumikawa, Marcus Conrad, Shiro Bannai, Hideyo Sato

    Scientific Reports8 ( 1 )   2018年12月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Nature Publishing Group  

    System xc - was recently described as the most upstream node in a novel form of regulated necrotic cell death, called ferroptosis. In this context, the small molecule erastin was reported to target and inhibit system xc -, leading to cysteine starvation, glutathione depletion and consequently ferroptotic cell death. Although the inhibitory effect of erastin towards system xc - is well-documented, nothing is known about its mechanism of action. Therefore, we sought to interrogate in more detail the underlying mechanism of erastin's pro-ferroptotic effects. When comparing with some well-known inhibitors of system xc -, erastin was the most efficient inhibitor acting at low micromolar concentrations. Notably, only a very short exposure of cells with low erastin concentrations was sufficient to cause a strong and persistent inhibition of system xc -, causing glutathione depletion. These inhibitory effects towards system xc - did not involve cysteine modifications of the transporter. More importantly, short exposure of tumor cells with erastin strongly potentiated the cytotoxic effects of cisplatin to efficiently eradicate tumor cells. Hence, our data suggests that only a very short pre-treatment of erastin suffices to synergize with cisplatin to efficiently induce cancer cell death, findings that might guide us in the design of novel cancer treatment paradigms.

    DOI: 10.1038/s41598-018-19213-4

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    その他リンク: http://www.nature.com/articles/s41598-018-19213-4.pdf

  • Cystine/glutamate transporter, system xc −, is involved in nitric oxide production in mouse peritoneal macrophages 査読

    Sho Kobayashi, Shinji Hamashima, Takujiro Homma, Mami Sato, Ryosuke Kusumi, Shiro Bannai, Junichi Fujii, Hideyo Sato

    Nitric Oxide - Biology and Chemistry78   32 - 40   2018年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Academic Press Inc.  

    The amino acid transport system xc − is important for maintaining intracellular glutathione levels and extracellular redox balance. The main component of system xc −, xCT, is strongly induced by various stimuli, including oxidative stress and bacterial lipopolysaccharides (LPS) in macrophages. In the present study, we investigated the production of nitric oxide by LPS-stimulated mouse peritoneal macrophages isolated from both xCT-deficient and wild-type mice. After culturing macrophages in the presence of LPS for 24–48 h, nitrite levels in the medium of xCT-deficient macrophages were significantly decreased compared to that of wild-type cells. However, the transport activity of arginine, a precursor of nitric oxide, and the expression of nitric oxide synthase 2 in xCT-deficient macrophages were similar to those of wild-type cells. When wild-type macrophages were cultured in the medium that contained no cystine, nitric oxide production was decreased to the level similar to that of the xCT-deficient macrophages. When xCT-deficient macrophages were cultured with 2-mercaptoethanol, intracellular cysteine levels were increased and nitrite accumulation in the medium was significantly increased. On the other hand, when these cells were cultured with buthionine sulfoximine, an inhibitor of glutathione synthesis, nitrite accumulation in the medium was essentially unchanged, although intracellular glutathione levels were very low. Reactive oxygen species levels in xCT-deficient macrophages were higher than those of wild-type cells, and treatment with LPS caused an increase in oxidative stress in both cells. These results suggest that intracellular cysteine supplied by xCT contributes to nitric oxide production and the reduction of oxidative stress in macrophages.

    DOI: 10.1016/j.niox.2018.05.005

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  • Adsorption of Protein-Bound Uremic Toxins Through Direct Hemoperfusion With Hexadecyl-Immobilized Cellulose Beads in Patients Undergoing Hemodialysis 査読

    Suguru Yamamoto, Mami Sato, Yoko Sato, Takuya Wakamatsu, Yoshimitsu Takahashi, Akira Iguchi, Kentaro Omori, Yasushi Suzuki, Isei Ei, Yoshikatsu Kaneko, Shin Goto, Junichiro J. Kazama, Fumitake Gejyo, Ichiei Narita

    Artificial Organs42 ( 1 ) 88 - 93   2018年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Blackwell Publishing Inc.  

    An accumulation of protein-bound uremic toxins (PBUTs) is one of major reasons for development of uremia-related complications. We examined the PBUT removal ability of a hexadecyl-immobilized cellulose bead (HICB)-containing column for patients undergoing hemodialysis. Adsorption of indoxyl sulfate (IS), a representative PBUT, to HICBs was examined in vitro. The HICB column was used in patients undergoing hemodialysis for direct hemoperfusion with a regular hemodialyzer. The serum IS, indole acetic acid (IAA), phenyl sulfate (PhS), and p-cresyl sulfate (PCS) levels were measured before and after passing the column. HICBs adsorbed protein-free (free) IS in a dose- and time-dependent manner in vitro (55.4 ± 1.4% adsorption of 1 millimolar, 251 µg/mL, IS for 1 h). In clinical studies, passing the HICB-containing column decreased the serum level of free IS, IAA, PhS, and PCS levels significantly (by 34.4 ± 30.0%, 34.8 ± 25.4%, 28.4 ± 18.0%, and 34.9 ± 22.1%, respectively), but not protein-bound toxins in maintenance hemodialysis patients. HICBs absorbed some amount of free PBUTs, but the clinical trial to use HICB column did not show effect to reduce serum PBUTs level in hemodialysis patients. Adsorption treatment by means of direct hemoperfusion with regular hemodialysis may become an attractive blood purification treatment to increase PBUT removal when more effective materials to adsorb PBUTs selectively will be developed.

    DOI: 10.1111/aor.12961

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  • Cystathionine is a novel substrate of cystine/glutamate transporter: Implications for immune function implications for immune function 査読

    Sho Kobayashi, Mami Sato, Takayuki Kasakoshi, Takumi Tsutsui, Masahiro Sugimoto, Mitsuhiko Osaki, Futoshi Okada, Kiharu Igarashi, Jun Hiratake, Takujiro Homma, Marcus Conrad, Junichi Fujii, Tomoyoshi Soga, Shiro Bannai, Hideyo Sato

    Journal of Biological Chemistry290 ( 14 ) 8778 - 8788   2015年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:American Society for Biochemistry and Molecular Biology Inc.  

    The cystine/glutamate transporter, designated as system x&lt
    inf&gt
    c&lt
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    &lt
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    , is important for maintaining intracellular glutathione levels and extracellular redox balance. The substrate-specific component of system x&lt
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    , xCT, is strongly induced by various stimuli, including oxidative stress, whereas it is constitutively expressed only in specific brain regions and immune tissues, such as the thymus and spleen. Although cystine and glutamate are the well established substrates of system x&lt
    inf&gt
    c&lt
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    &lt
    sup&gt
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    and the knockout of xCT leads to alterations of extracellular redox balance, nothing is known about other potential substrates. We thus performed a comparative metabolite analysis of tissues from xCT-deficient and wild-type mice using capillary electrophoresis time-of-flight mass spectrometry. Although most of the analyzed metabolites did not show significant alterations between xCT-deficient and wild-type mice, cystathionine emerged as being absent specifically in the thymus and spleen of xCT-deficient mice. No expression of either cystathionine β-synthase or cystathionine γ-lyase was observed in the thymus and spleen of mice. In embryonic fibroblasts derived from wild-type embryos, cystine uptake was significantly inhibited by cystathionine in a concentration-dependent manner. Wild-type cells showed an intracellular accumulation of cystathionine when incubated in cystathionine-containing buffer, which concomitantly stimulated an increased release of glutamate into the extracellular space. By contrast, none of these effects could be observed in xCT-deficient cells. Remarkably, unlike knock-out cells, wild-type cells could be rescued from cystine deprivation-induced cell death by cystathionine supplementation.Wethus conclude that cystathionine is a novel physiological substrate of system x&lt
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    and that the accumulation of cystathionine in immune tissues is exclusively mediated by system x&lt
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    &lt
    sup&gt
    -&lt
    /sup&gt
    .

    DOI: 10.1074/jbc.M114.625053

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▶ 全件表示

受賞

  • first prize for short talks

    2018年12月   the 2018 Cold Spring Harbor Asia conference on Iron, Reactive OxygenSpecies & Ferroptosis in Life, Death & Disease   The cystine/glutamate antiporter is essential for maintaining the highly metastatic potential of B16F10 skin melanoma cells.

    Sato M(発表者/筆頭著者), Onuma K, Costa da Silva M, Kusumi R, Osaki M, Feederle R, Bannai S, Conrad M, Okada F, Sato H

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