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Effect of MCP-1 and sSiglec9 in the animal models of acute liver failure

Research Project

Project/Area Number 18K07936
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 53010:Gastroenterology-related
Research InstitutionNagoya University

Principal Investigator

Ishigami Masatoshi  名古屋大学, 医学系研究科, 准教授 (90378042)

Project Period (FY) 2018-04-01 – 2022-03-31
Project Status Completed (Fiscal Year 2021)
Budget Amount *help
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2021: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2020: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2019: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Keywords肝再生 / マクロファージ / 炎症-再生相関 / 急性肝不全 / 動物モデル / MCP-1 / sSiglec-9 / sSiglec-9 / 抗炎症 / 炎症抑制
Outline of Final Research Achievements

In this study, we investigated the effect of combination of 2 humoral factors; MCP-1, which is the well-known factors for the migration of macrophage into inflamed site, and sSiglec-9, which is the key factor of transition of macrophage from inflammatory to anti-inflammatory subset in several animal models of acute liver injury as the candidate for promoting liver regeneration directly, which does not exist in clinical practice.
Combination of these 2 factors improved the survival of mice in Concanavalin A or CCl4 induced acute liver injury models. Expression of CD206 and Arginase-1, which are the surface markers of anti-inflammatory subsets of macrophage and HGF, β-catenin, or EpCAM, which are the markers of liver regeneration, increased in the group of inoculation of these 2 factors compared with controls. In cultured hepatic stellate cells, these 2 factors inhibit the activation, and keep the quiescent state, resulting the increased expression of HGF.

Academic Significance and Societal Importance of the Research Achievements

現在、急性肝不全においてその治癒の鍵となる肝再生促進を直接促進させる薬剤は存在せず、そのために未だに多くの患者を失っているのが現状である。その一つの有力な候補としてMCP-1+sSiglec9の2因子併用が、多くの肝不全動物モデルにおいて有用であること、またその炎症抑制、肝再生促進のメカニズムを明らかにすることで、現在実臨床で存在しない新たな治療法、および現在でも死亡率の高い本疾患における生存率の向上に寄与することが可能となってくるであろう。

Report

(5 results)
  • 2021 Annual Research Report   Final Research Report ( PDF )
  • 2020 Research-status Report
  • 2019 Research-status Report
  • 2018 Research-status Report
  • Research Products

    (1 results)

All 2020

All Presentation (1 results)

  • [Presentation] マウスNASHモデルに対する歯髄由来幹細胞培養上清の抗線維化作用の検討2020

    • Author(s)
      武藤 久哲、伊藤 隆徳、石上 雅敏、藤城 光弘
    • Organizer
      第41回日本炎症・再生医学会
    • Related Report
      2020 Research-status Report

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Published: 2018-04-23   Modified: 2023-01-30  

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