研究者データベース

江口 遼太(エグチ リヨウタ)
獣医学研究院 獣医学部門 基礎獣医科学分野
助教

基本情報

所属

  • 獣医学研究院 獣医学部門 基礎獣医科学分野

職名

  • 助教

学位

  • 博士(獣医学)(北海道大学)

科研費研究者番号

  • 10846067

J-Global ID

研究分野

  • ライフサイエンス / 薬理学
  • ライフサイエンス / 獣医学

職歴

  • 2019年04月 - 現在 北海道大学 大学院獣医学研究院 基礎獣医科学分野 薬理学教室 助教
  • 2016年04月 - 2019年03月 北海道大学 大学院獣医学研究科 日本学術振興会特別研究員DC1

学歴

  •         - 2019年   北海道大学   大学院獣医学研究科   修了
  •         - 2015年   北海道大学   獣医学部   卒業

所属学協会

  • 日本薬理学会   日本獣医学会   

研究活動情報

論文

  • Kohei Morimoto, Taisuke Kitano, Ryota Eguchi, Ken-Ichi Otsuguro
    Biochemical and biophysical research communications 2020年05月22日 [査読有り][通常論文]
     
    Noradrenaline (NA) suppresses TNF-α production via β-adrenoceptors (ARs) in brain astrocytes. However, the downstream pathways from β-ARs, and the involvement of α-ARs, remains unknown. In this study, we investigated the AR-mediated regulation of TNF-α mRNA levels in cultured astrocytes from rat spinal cord. NA, the α1-agonist phenylephrine, and the β-agonist isoproterenol decreased the TNF-α mRNA level, while the α2-agonist dexmedetomidine increased it. The isoproterenol-induced TNF-α mRNA decrease was accompanied by a decrease in ERK phosphorylation. An adenylyl cyclase activator and an ERK inhibitor mimicked these effects. These results indicate that the transcriptional regulation of TNF-α by β-ARs is mediated via cAMP pathways followed by the ERK pathway inhibition. The dexmedetomidine-induced TNF-α mRNA increase was accompanied by phosphorylation of JNK and ERK, which was blocked by a JNK inhibitor. Furthermore, the LPS-induced increase in the TNF-α mRNA level was accompanied by NF-κB nuclear translocation, and both these effects were blocked by phenylephrine. An NF-κB inhibitor suppressed the LPS-induced increase in the TNF-α mRNA level. These results suggest that α1-ARs suppress the LPS-induced increase in the TNF-α mRNA level via inhibition of NF-κB nuclear translocation. Taken together, our study reveals that both α- and β-ARs are involved in the transcriptional regulation of TNF-α in astrocytes.
  • Eguchi R, Yamaguchi S, Otsuguro KI
    Journal of pharmacological sciences 139 2 98 - 104 2019年02月 [査読有り][通常論文]
  • Ujike A, Kuraishi T, Yamaguchi S, Eguchi R, Kitano T, Kamise J, Ito S, Otsuguro KI
    European journal of pharmacology 821 88 - 96 2018年02月15日 [査読有り][通常論文]
     
    H2S has excitatory and inhibitory effects on Ca2+ signals via transient receptor potential ankyrin 1 (TRPA1) and ATP-sensitive K+ channels, respectively. H2S converts intracellularly to polysulfides, which are more potent agonists for TRPA1 than H2S. Under inflammatory conditions, changes in the expression and activity of these H2S target channels and/or the conversion of H2S to polysulfides may modulate H2S effects. Effects of proinflammatory cytokines on H2S-induced Ca2+ signals and polysulfide production in RIN14B cells were examined using fluorescence imaging with fura-2 and SSP4, respectively. Na2S, a H2S donor, induced 1) the inhibition of spontaneous Ca2+ signals, 2) inhibition followed by [Ca2+]i increase, and 3) rapid [Ca2+]i increase without inhibition in 50% (23/46), 22% (10/46), and 17% (8/46) of cells tested, respectively. IL-1β augmented H2S-induced [Ca2+]i increases, which were inhibited by TRPA1 and voltage-dependent L-type Ca2+ channel blockers. However, IL-1β treatment did not affect [Ca2+]i increases evoked by a TRPA1 agonist or high concentration of KCl. Na2S increased intracellular polysulfide levels, which were enhanced by IL-1β treatment. A NOS inhibitor suppressed the increased polysulfide production and [Ca2+]i increase in IL-1β-treated cells. These results suggest that IL-1β augments H2S-induced [Ca2+]i increases via the conversion of H2S to polysulfides through NO synthesis, but not via changes in the activity and expression of target channels. Polysulfides may play an important role in the effects of H2S during inflammation.
  • Ryota Eguchi, Sanae Akao, Ken-ichi Otsuguro, Soichiro Yamaguchi, Shigeo Ito
    JOURNAL OF PHARMACOLOGICAL SCIENCES 128 1 47 - 53 2015年05月 [査読有り][通常論文]
     
    Extracellular adenosine is a neuromodulator in the central nervous system. Astrocytes mainly participate in adenosine production, and extracellular adenosine accumulates under physiological and pathophysiological conditions. Inhibition of intracellular adenosine metabolism and reduction of the external Ca2+ concentration ([Ca2+](e)) participate in adenosine accumulation, but the precise mechanisms remain unclear. This study investigated the mechanisms underlying extracellular adenosine accumulation in cultured rat spinal astrocytes. The combination of adenosine kinase and deaminase (ADK/ADA) inhibition and a reduced [Ca2+](e) increased the extracellular adenosine level. ADK/ADA inhibitors increased the level of extracellular adenosine but not of adenine nucleotides, which was suppressed by inhibition of equilibrative nucleoside transporter (ENT) 2. Unlike ADK/ADA inhibition, a reduced [Ca2+](e) increased the extracellular level not only of adenosine but also of ATP. This adenosine increase was enhanced by ENT2 inhibition, and suppressed by sodium polyoxotungstate (ecto-nucleoside triphosphate diphosphohydrolase inhibitor). Gap junction inhibitors suppressed the increases in adenosine and adenine nucleotide levels by reduction of [Ca2+](e). These results indicate that extracellular adenosine accumulation by ADK/ADA inhibition is due to the adenosine release via ENT2, while that by reduction of [Ca2+] e is due to breakdown of ATP released via gap junction hemichannels, after which ENT2 incorporates adenosine into the cells. (C) 2015 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.

受賞

  • 2017年09月 日本比較薬理学・毒性学会 平成29年度日本比較薬理学・毒性学会奨励賞
     低Ca2+によるアストロサイトの細胞外アデノシン蓄積に対するFGF2の影響 
    受賞者: 江口 遼太

共同研究・競争的資金等の研究課題

  • 抗うつ薬によるアストロサイトのプリン放出・代謝機能変化の解析
    日本学術振興会:研究活動スタート支援
    研究期間 : 2019年10月 -2021年09月 
    代表者 : 江口 遼太


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