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Specially Appointed Associate Professor |
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1-1-1 Sakuragaoka, Setagaya-ku, Tokyo, 156-8502, Japan |
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Shigeru TANABE Specially Appointed Associate Professor |
Employment Record in Research 【 display / non-display 】
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Tokyo University of Agriculture Nodai Research Institute Tokyo NODAI Research Institute (TNRI) Specially Appointed Associate Professor
2023.04
Country：Japan
Professional Memberships 【 display / non-display 】
Research Areas 【 display / non-display 】
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Life Science / Physiology
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Life Science / Clinical pharmacy
Papers 【 display / non-display 】
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Accumulation of autofluorescent storage material in brain is accelerated by ischemia in chloride channel 3 gene-deficient mice Reviewed International journal
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 2012.11
Language：English Publishing type：Research paper (scientific journal)
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 Reviewed International journal
Y. Okada, T. Shimizu, E. Maeno, S. Tanabe, X. Wang, N. Takahashi
Journal of Membrane Biology 209 ( 1 ) 21 - 29 2006.01
Language：English Publishing type：Research paper (scientific journal)
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.
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HCO <inf>3</inf><sup>-</sup>-independent rescue from apoptosis by stilbene derivatives in rat cardiomyocytes Reviewed International journal
Shigeru Tanabe, Xiaoming Wang, Nobuyuki Takahashi, Hiromi Uramoto, Yasunobu Okada
FEBS Letters 579 ( 2 ) 517 - 522 2005.01
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal)
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.
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ClC-3-independent sensitivity of apoptosis to Cl <sup>-</sup> channel blockers in mouse cardiomyocytes Reviewed International journal
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
Language：English Publishing type：Research paper (scientific journal)
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 Reviewed International journal
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
Language：English Publishing type：Research paper (scientific journal)
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.
Books and Other Publications 【 display / non-display 】
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Center for Research and Development Strategy, Japan Science and Technology Agency 2021.09 （ ISBN:9784888907613 ）
Total pages：46 Language：Japanese Book type：Report
Misc 【 display / non-display 】
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Cl- channel distinct from ClC-3 is a target of stilbene derivative for suppression of cardiomyocyte apoptosis International journal
N. Takahashi, X. Wang, S. Tanabe, H. Uramoto, K. Jishage, S. Uchida, S. Sasaki, Y. Okada
Japanese Journal of Physiology 55(Suppl):S75 2005
Language：English Publishing type：Research paper, summary (national, other academic conference)
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Volume-sensitive chloride currents in cardiomyocytes isolated from ClC-3 knockout mice International journal
H. Xu, W. Gong, T. Shimizu, S. Tanabe, S. Uchida, S. Sasaki, Y. Okada
Japanese Journal of Physiology 54(Suppl):S68 2004
Language：English Publishing type：Research paper, summary (national, other academic conference)
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Role of Cl- channel in apoptosis induction International journal
Y. Okada, T. Shimizu, E. Maeno. S. Tanabe
Japanese Journal of Physiology 53(Suppl):S55 2003
Language：English Publishing type：Research paper, summary (national, other academic conference)
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Role of Cl- channel in apoptosis induction International journal
Y. Okada, T. Shimizu, E. Maeno, S. Tanabe
Journal of Pharmacological Sciences 91(Suppl 1):31P 2003
Language：English Publishing type：Research paper, summary (national, other academic conference)
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Prevention of staurosporine-induced apoptotic cell death by DIDS and SITS in rat cardiomyocytes in primary culture International journal
S. Tanabe, E. Maeno, Y. Okada
Japanese Journal of Physiology 52(Suppl):S34 2002
Authorship：Lead author Language：English Publishing type：Research paper, summary (national, other academic conference)
Industrial Property Rights 【 display / non-display 】
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心疾患治療剤
岡田 泰伸, 田辺 秀
Applicant：中外製薬株式会社
Application no：JP2002008069 Date applied：2002.08
Publication no：WO2003-014727 Date published：2003.02
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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
Applicant：シー・アンド・シー・リサーチ・ラブズ
Application no：JP1995001138 Date applied：1995.06
Publication no：WO1996-004231 Date published：1996.02
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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
Applicant：シー・アンド・シー・リサーチ・ラブズ
Application no：JP1995001137 Date applied：1995.06
Publication no：WO1996-006084 Date published：1996.02
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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
Applicant：シー・アンド・シー・リサーチ・ラブズ
Application no：JP1995001134 Date applied：1995.06
Publication no：WO1996-005174 Date published：1996.02