2023/09/25 更新

写真b

田辺 秀 (タナベ シゲル)

Shigeru TANABE

特命准教授

職名

特命准教授

研究室住所

東京都世田谷区桜丘1-1-1

ホームページ

https://www.nodai.ac.jp/

外部リンク

学位 【 表示 / 非表示

  • 博士(理学) ( 1992年03月   岡山大学 )

学内職務経歴 【 表示 / 非表示

  • 東京農業大学   総合研究所   総合研究所   特命准教授

    2023年04月 - 現在

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    国名:日本国

所属学協会 【 表示 / 非表示

研究分野 【 表示 / 非表示

  • ライフサイエンス / 生理学

  • ライフサイエンス / 医療薬学

論文 【 表示 / 非表示

  • Accumulation of autofluorescent storage material in brain is accelerated by ischemia in chloride channel 3 gene-deficient mice 査読あり 国際誌

    Hirokazu Ohtaki, Kenji Ohara, Dandan Song, Kazuyuki Miyamoto, Tomomi Tsumuraya, Sachiko Yofu, Kenji Dohi, Shigeru Tanabe, Sei Sasaki, Shinichi Uchida, Masaji Matsunaga, Seiji Shioda

    Journal of Neuroscience Research   90 ( 11 )   2163 - 2172   2012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)  

    Autofluorescent storage material (ASM) is an aging pigment that accumulates during the normal course of senescence. Although the role of ASM has yet to be fully elucidated, ASM has been implicated in age-related neurodegeneration. In this study, we determined the level of ASM in chloride channel 3 (ClC-3) gene-deficient (KO) mice both in response to aging and following mild global ischemia. To understand the mechanism of action of the ASM, mice subjected to ischemia were treated with the cyclooxygenase (COX) inhibitor indomethacin or with the noncompetitive glutamate receptor antagonist MK-801. ClC-3 KO mice displayed age-related neurodegeneration of the neocortex as well as the hippocampus. The cortical layers in particular granular layers became thinner with aging. ASM accumulated in the brains of ClC-3 KO mice was increased seven- to 50-fold over that observed in the corresponding regions of their wild-type littermates. Young wild-type mice survived longer than age-matched ClC-3 KO mice after permanent global ischemia. However, in the case of older animals, the survival curves were similar. The ASM also increased four- to fivefold 10 days after mild global ischemia, an effect that was suppressed by treatment with indomethacin and MK-801. These results suggest that temporary ischemia might trigger a process similar to aging in the brain, mimicking the effect of age-related neurodegenerative diseases. © 2012 Wiley Periodicals, Inc.

    DOI: 10.1002/jnr.23110

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  • Volume-sensitive chloride channels involved in apoptotic volume decrease and cell death 査読あり 国際誌

    Y. Okada, T. Shimizu, E. Maeno, S. Tanabe, X. Wang, N. Takahashi

    Journal of Membrane Biology   209 ( 1 )   21 - 29   2006年01月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Apoptosis is an essential process in organ development, tissue homeostasis, somatic cell turnover, and the pathogenesis of degenerative diseases. Apoptotic cell death occurs in response to a variety of stimuli in physiological and pathological circumstances. Efflux of K+ and Cl- leads to apoptotic volume decrease (AVD) of the cell. Both mitochondrion-mediated intrinsic, and death receptor-mediated extrinsic, apoptotic stimuli have been reported to rapidly activate Cl- conductances in a large variety of cell types. In epithelial cells and cardiomyocytes, the AVD-inducing anion channel was recently determined to be the volume-sensitive outwardly rectifying (VSOR) Cl- channel which is usually activated by swelling under non-apoptotic conditions. Blocking the VSOR Cl- channel prevented cell death in not only epithelial and cardiac cells, but also other cell types, by inhibiting the induction of AVD and subsequent apoptotic events. Ischemia-reperfusion-induced apoptotic death in cardiomyocytes and brain neurons was also prevented by Cl- channel blockers. Furthermore, cancer cell apoptosis induced by the anti-cancer drug cisplatin was recently found to be associated with augmented activity of the VSOR Cl- channel and to be inhibited by a Cl- channel blocker. The apoptosis-inducing VSOR Cl- channel is distinct from ClC-3 and its molecular identity remains to be determined. © Springer Science+Business Media, Inc. 2006.

    DOI: 10.1007/s00232-005-0836-6

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  • HCO <inf>3</inf><sup>-</sup>-independent rescue from apoptosis by stilbene derivatives in rat cardiomyocytes 査読あり 国際誌

    Shigeru Tanabe, Xiaoming Wang, Nobuyuki Takahashi, Hiromi Uramoto, Yasunobu Okada

    FEBS Letters   579 ( 2 )   517 - 522   2005年01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)  

    Apoptosis of rat cardiomyocytes induced by staurosporine is prevented by a stilbene derivative (DIDS), which is a known blocker of both Cl-/HCO3- exchangers and Cl - channels. To clarify its target, staurosporine-induced activation of caspase-3, DNA laddering and cell death were examined in cultured rat cardiomyocytes. Removal of ambient HCO3-, which minimizes the function of Cl-/HCO3- exchangers, failed to affect the preventive effect of DIDS on apoptosis. A carboxylate analog Cl - channel blocker, which does not block Cl-/HCO3- exchangers, also inhibited apoptotic events. Thus, rescue by DIDS of cardiomyocytes from apoptosis is mediated by blockage of Cl - channels. © 2004 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

    DOI: 10.1016/j.febslet.2004.12.020

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  • ClC-3-independent sensitivity of apoptosis to Cl <sup>-</sup> channel blockers in mouse cardiomyocytes 査読あり 国際誌

    Nobuyuki Takahashi, Xiaoming Wang, Shigeru Tanabe, Hiromi Uramoto, Kouichi Jishage, Shinichi Uchida, Sei Sasaki, Yasunobu Okada

    Cellular Physiology and Biochemistry   15 ( 6 )   263 - 270   2005年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    It has been shown that Cl - /HCO 3- exchangers and Cl - channels, both of which are sensitive to stilbene derivatives, have essential roles in the mechanism of apoptosis induction. Staurosporine-induced apoptosis in neonatal mouse cardiomyocytes was prevented by a stilbene derivative, DIDS. To clarify whether Cl - /HCO 3- exchangers or Cl - channels are targets of DIDS and whether ClC-3 is involved in the apoptotic process, staurosporine-induced reduction of cell viability, DNA laddering and caspase-3 activation were examined in cultured mouse ventricular myocytes derived from wild-type and ClC-3-deficient mice. Staurosporine-induced apoptosis and its DIDS sensitivity in ambient HCO 3- -free conditions in which operation of Cl - /HCO 3- exchangers is minimized were indistinguishable from when HCO 3- was present. Apoptosis was also prevented by application of a non-stilbene-derivative Cl - channel blocker, NPPB, which cannot block Cl - / HCO 3- exchangers. Cardiomyocytes derived from ClC-3-deficient mice similarly underwent apoptosis after exposure to staurosporine; moreover, apoptosis was prevented by application of DIDS or NPPB. Thus, we conclude that in cardiomyocytes, apoptosis is critically dependent on operation not of Cl - /HCO 3- exchangers but of Cl - channels which are distinct from ClC-3. Copyright © 2005 S. Karger AG.

    DOI: 10.1159/000087236

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  • Single-channel properties of volume-sensitive Cl<sup>-</sup> channel in ClC-3-deficient cardiomyocytes 査読あり 国際誌

    Jun Wang, Hongtao Xu, Shigeru Morishima, Shigeru Tanabe, Kouichi Jishage, Shinichi Uchida, Sci Sasaki, Yasunobu Okada, Takahiro Shimizu

    Japanese Journal of Physiology   55 ( 6 )   379 - 383   2005年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    It is controversial whether the ClC-3 protein, which is one of the voltage-dependent chloride channel ClC family members, is a candidate for the volume-sensitive outwardly rectifying (VSOR) Cl- channel per se or its regulator. Here, for the first time, we examined the single-channel properties of the VSOR Cl- channel in ventricular myocytes isolated from ClC-3 - deficient mice. The single-channel current induced by cell swelling exhibited Cl- selectivity, mild outward rectification, and an intermediate unitary conductance (around 38 pS). A Cl- channel blocker, 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS), reversibly inhibited the outward current. These single-channel properties were identical with those in ClC-3 expressing wild-type ventricular myocytes. These results indicate that the single-channel activity of the VSOR Cl- channel is independent of the expression of ClC-3 proteins in mouse ventricular myocytes.

    DOI: 10.2170/jjphysiol.S655

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  • 戦略プロポーザル 生体感覚システム ~受容からの統合的理解と制御に向けた 基盤技術の創出~

    永井 良三・谷口 維紹・山原 恵子・辻 真博・中村 輝郎・宮薗 侑也・桑原 明日香・井上 貴文・荒岡 礼・田辺 秀

    国立研究開発法人科学技術振興機構 研究開発戦略センター (CRDS)  2021年09月  ( ISBN:9784888907613

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    総ページ数:46   記述言語:日本語   著書種別:調査報告書

    本プロポーザルは、生体内外の情報を受容する感覚器および臓器と末梢神経ネットワークで構成されるヒトの生体感覚システムを統合的に理解し、その理解に基づく制御に向けた基盤技術を創出することにより、疾病予防と健康増進、疾患の新規治療戦略の創出などに寄与するための研究開発戦略を提言する。

MISC 【 表示 / 非表示

  • Cl- channel distinct from ClC-3 is a target of stilbene derivative for suppression of cardiomyocyte apoptosis 国際誌

    N. Takahashi, X. Wang, S. Tanabe, H. Uramoto, K. Jishage, S. Uchida, S. Sasaki, Y. Okada

    Japanese Journal of Physiology 55(Suppl):S75   2005年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(全国大会,その他学術会議)  

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  • Volume-sensitive chloride currents in cardiomyocytes isolated from ClC-3 knockout mice 国際誌

    H. Xu, W. Gong, T. Shimizu, S. Tanabe, S. Uchida, S. Sasaki, Y. Okada

    Japanese Journal of Physiology 54(Suppl):S68   2004年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(全国大会,その他学術会議)  

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  • Role of Cl- channel in apoptosis induction 国際誌

    Y. Okada, T. Shimizu, E. Maeno. S. Tanabe

    Japanese Journal of Physiology 53(Suppl):S55   2003年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(全国大会,その他学術会議)  

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  • Role of Cl- channel in apoptosis induction 国際誌

    Y. Okada, T. Shimizu, E. Maeno, S. Tanabe

    Journal of Pharmacological Sciences 91(Suppl 1):31P   2003年

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(全国大会,その他学術会議)  

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  • Prevention of staurosporine-induced apoptotic cell death by DIDS and SITS in rat cardiomyocytes in primary culture 国際誌

    S. Tanabe, E. Maeno, Y. Okada

    Japanese Journal of Physiology 52(Suppl):S34   2002年

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究発表ペーパー・要旨(全国大会,その他学術会議)  

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産業財産権 【 表示 / 非表示

  • 心疾患治療剤

    岡田 泰伸, 田辺 秀

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    出願人:中外製薬株式会社

    出願番号:JP2002008069  出願日:2002年08月

    公表番号:WO2003-014727  公表日:2003年02月

    J-GLOBAL

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  • 新規なアミン誘導体、その製造方法及び抗不整脈剤としての用途

    チョン ユウ ソプ, キム ハク ヨプ, ジョン キョン ユン, ミン ジェ キ, 田辺 秀

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    出願人:シー・アンド・シー・リサーチ・ラブズ

    出願番号:JP1995001138  出願日:1995年06月

    公表番号:WO1996-004231  公表日:1996年02月

    J-GLOBAL

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  • 新規なキノリルアミン誘導体、その製造方法及び抗不整脈剤としての用途

    チョン ユウ ソプ, キム ドン イク, ジョン ギ ホ, キム カブ シク, 田辺 秀, 小園 敏郎

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    出願人:シー・アンド・シー・リサーチ・ラブズ

    出願番号:JP1995001137  出願日:1995年06月

    公表番号:WO1996-006084  公表日:1996年02月

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  • 新規なアミン誘導体、その製造方法及び抗不整脈剤としての用途

    チョン ユウ ソプ, パク ソン デ, クォン レー ソン, シン ホン ソブ, 田辺 秀

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    出願人:シー・アンド・シー・リサーチ・ラブズ

    出願番号:JP1995001134  出願日:1995年06月

    公表番号:WO1996-005174  公表日:1996年02月

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委員歴 【 表示 / 非表示

  • 日本生理学会   評議員  

    1998年03月 - 現在   

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    団体区分:学協会

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