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The role of molecular chaperone VCP in excitotoxin-induced cell death.

Research Project

Project/Area Number 16K10112
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Embryonic/Neonatal medicine
Research InstitutionSuzuka University of Medical Science

Principal Investigator

Furukawa Ayako  鈴鹿医療科学大学, 薬学部, 助教 (10455537)

Co-Investigator(Kenkyū-buntansha) 郡山 恵樹  鈴鹿医療科学大学, 薬学部, 准教授 (70397199)
Research Collaborator CHIBA yoichi  
Project Period (FY) 2016-04-01 – 2019-03-31
Project Status Completed (Fiscal Year 2018)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords興奮毒性 / VCP / 酸化ストレス / 細胞死 / アストロサイト / 神経細胞死 / 活性化アストロサイト / 活性化アストロサイ / シャペロンタンパク質 / カルボニル化
Outline of Final Research Achievements

In the present study, we focused on the role of valosin containing protein(VCP) in excitotoxin-induced cell death. We elucidated that VCP was increased in reactive astrocyte in excitotoxin-treated rat hippocampus. In primary mixed glial cultures, Eeyarestatin I, which is an inhibitor of VCP, was shown to promote cell death by glutamate. These results suggest that VCP may act as a cytoprotective factor in glial cells. Eeyarestatin I induced ER stress marker proteins in glial cells, no induction of them were observed in eeyarestatin and glutamate-treated cells. Thus, the cytoprotective effect of VCP may not be an ER stress response.

Academic Significance and Societal Importance of the Research Achievements

興奮毒性は、神経細胞の過剰な興奮性シグナル伝達によって生じる。低酸素性虚血性脳症は、周産期の一過性の低酸素と虚血による興奮毒性をきっかけに、てんかんなどの後遺症を引き起こす。興奮毒性により、どのような分子が関与して脳内の環境が変化するのか、それらの分子が治療標的となり得るかを明らかにすることは、周産期の傷害をきっかけに生じる神経学的後遺症を改善する上で重要であると考える。

Report

(4 results)
  • 2018 Annual Research Report   Final Research Report ( PDF )
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (7 results)

All 2018 2017 2016

All Journal Article (3 results) (of which Peer Reviewed: 3 results,  Open Access: 2 results) Presentation (4 results) (of which Int'l Joint Research: 2 results)

  • [Journal Article] S-Nitrosylation Regulates Cell Survival and Death in the Central Nervous System.2018

    • Author(s)
      Koriyama Y, Furukawa A.
    • Journal Title

      Neurochem Res.

      Volume: 43 Issue: 1 Pages: 41-49

    • DOI

      10.1007/s11064-017-2303-z

    • Related Report
      2017 Research-status Report
    • Peer Reviewed
  • [Journal Article] A role of heat shock protein 70 in photoreceptor cell death: potential as a novel therapeutic target in retinal degeneration.2016

    • Author(s)
      Furukawa A, Koriyama Y.
    • Journal Title

      CNS Neurosci. Ther.

      Volume: 22 Issue: 1 Pages: 7-14

    • DOI

      10.1111/cns.12471

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] HSP70 cleavage-induced photoreceptor cell death caused by N-methyl-N-nitrosourea.2016

    • Author(s)
      Koriyama Y, Furukawa A.
    • Journal Title

      Neural Regeneration Research

      Volume: 11 Issue: 11 Pages: 1758-1759

    • DOI

      10.4103/1673-5374.194721

    • Related Report
      2016 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] Comprehensive analysis of protein expression profiles in sclerotic hippocampus from patients with mesial temporal lobe epilepsy.2018

    • Author(s)
      Furukawa A, Kakita A, Chiba Y, Kameyama S, Shimada A
    • Organizer
      19th International Congress of Neuropathology (ICN)
    • Related Report
      2018 Annual Research Report
    • Int'l Joint Research
  • [Presentation] グルタミン酸によるグリア細胞死誘導におけるグルタチオン減少とGRP78発現増加の役割2017

    • Author(s)
      古川絢子、松野夏紀、樋口善博
    • Organizer
      第90回日本生化学会大会
    • Related Report
      2017 Research-status Report
  • [Presentation] Novel photoreceptor cell death mechanism through calpain-dependent HSP70 cleavage2016

    • Author(s)
      Ayako Furukawa, Yoshiki Koriyama
    • Organizer
      XVII international symposium on retinal degeneration RD2016
    • Place of Presentation
      Kyoto
    • Year and Date
      2016-09-20
    • Related Report
      2016 Research-status Report
    • Int'l Joint Research
  • [Presentation] グルタミン酸によるグリア障害に関わる酸化損傷タンパク質の同定2016

    • Author(s)
      古川絢子、細井礼子、樋口善博
    • Organizer
      第89回日本生化学会大会
    • Place of Presentation
      仙台
    • Related Report
      2016 Research-status Report

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Published: 2016-04-21   Modified: 2020-03-30  

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