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Development of the new angiogenic inhibitor targeting HMGB-1

Research Project

Project/Area Number 15K18996
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field General pharmacology
Research InstitutionKindai University

Principal Investigator

KOBORI Takuro  近畿大学, 医学部, 助教 (60734697)

Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Keywordsマクロファージ / 血管新生 / 炎症性メディエーター / インターロイキン-18 / オステオポンチン / トロンビン / CD163 / 細胞間相互作用
Outline of Final Research Achievements

Macrophages (Mφs) are classified as M1 or M2 phenotypes, with the latter promoting angiogenesis which is a precipitating factor for several chronic inflammatory diseases including rheumatoid arthritis (RA) and various cancers. In this study, we initially established the simplified in vitro experimental model to evaluate the influence of micromilieu on the Mφ polarization status, morphology, and functional activity. As a result, M2-like Mφ strongly induced excessive angiogenesis through the direct cell-cell interaction with endothelial cells mediated by the surface CD163.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (7 results)

All 2018 2017 2016 2015 Other

All Journal Article (1 results) (of which Int'l Joint Research: 1 results,  Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (5 results) Remarks (1 results)

  • [Journal Article] Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to Excessive Angiogenesis.2018

    • Author(s)
      Kobori T, Hamasaki S, Kitaura A, Yamazaki Y, Nishinaka T, Niwa A, Nakao S, Wake H, Mori S, Yoshino T, Nishibori M, Takahashi H
    • Journal Title

      Frontiers in Immunology

      Volume: 9 Pages: 334-334

    • DOI

      10.3389/fimmu.2018.00334

    • Related Report
      2017 Annual Research Report
    • Peer Reviewed / Open Access / Int'l Joint Research
  • [Presentation] マクロファージと血管内皮細胞の細胞間相互作用による血管新生促進機構の解析2018

    • Author(s)
      小堀 宅郎、濱崎 真一、北浦 淳寛、山﨑 由衣、西中 崇、丹羽 淳子、西堀 正洋、髙橋 英夫
    • Organizer
      第 138 回 日本薬理学会関東部会
    • Related Report
      2017 Annual Research Report
  • [Presentation] IL-18 はオステオポンチンを介してマクロファージ M2 分化と血管新生作用を増強する2017

    • Author(s)
      小堀 宅郎、濱崎 真一、北浦 淳寛、西中 崇、丹羽 淳子、森 秀治、西堀 正洋、高橋 英夫
    • Organizer
      第 90 回 日本薬理学会年会
    • Place of Presentation
      長崎ブリックホールおよび長崎新聞文化ホール(長崎県長崎市)
    • Year and Date
      2017-03-15
    • Related Report
      2016 Research-status Report
  • [Presentation] IL-18 amplifies macrophage M2 polarization, leading to enhancement of angiogenesis via up-regulation of osteopontin2016

    • Author(s)
      Takuro Kobori, Takashi Nishinaka, Atsuko Niwa, Hideo Takahashi
    • Organizer
      12th International Conference on Protein Phosphatase
    • Place of Presentation
      近畿大学東大阪キャンパス(大阪府東大阪市)
    • Year and Date
      2016-10-27
    • Related Report
      2016 Research-status Report
  • [Presentation] M2 マクロファージによる血管新生促進作用に対する IL-18 の影響2016

    • Author(s)
      小堀 宅郎
    • Organizer
      第 89 回日本薬理学会年会
    • Place of Presentation
      神奈川県横浜市 パシフィコ横浜
    • Year and Date
      2016-03-09
    • Related Report
      2015 Research-status Report
  • [Presentation] IL-18 は M2 マクロファージによる血管新生を促進する2015

    • Author(s)
      小堀 宅郎
    • Organizer
      第 128 回日本薬理学会年会
    • Place of Presentation
      大阪府吹田市 千里ライフサイエンスセンター
    • Year and Date
      2015-11-20
    • Related Report
      2015 Research-status Report
  • [Remarks] 近畿大学 医学部 薬理学教室 ホームページ

    • URL

      http://www.med.kindai.ac.jp/pharma/

    • Related Report
      2017 Annual Research Report

URL: 

Published: 2015-04-16   Modified: 2020-01-20  

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