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Effects of IL-18 on pressure overloaded-heart

Research Project

Project/Area Number 26461136
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Cardiovascular medicine
Research InstitutionHyogo Medical University

Principal Investigator

Hirotani Shinichi  兵庫医科大学, 医学部, 講師 (20584220)

Co-Investigator(Kenkyū-buntansha) 岩破 俊博  兵庫医科大学, 医学部, 助教 (00648230)
西村 晃一  兵庫医科大学, 医学部, 病院助手 (30724116)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
KeywordsIL-18 / pressure overload / energy homeostasis / インターロイキン18 / 圧負荷 / エネルギー代謝 / 心不全 / 脂肪酸代謝 / LPL / 分子心臓病学 / 圧負荷ストレス
Outline of Final Research Achievements

Effects of IL-18 on pressure overloaded-heart have yet to be revealed. We introduced pressure overload by transverse aortic constriction (TAC) to wild type mice and IL-18 knockout mice. IL-18 knockout mice exhibited higher mortality and severer left ventricular remodeling after TAC. We examined myocardial AMPK activity. While TAC elevated AMPK activity in wild type heart, it did not in Il-18 heart. Therefore, we administered AMPK direct activator, AICAR, to IL-18 knockout mice. The administration attenuated higher mortality and severer left ventricular remodeling after TAC compared with wild type mice. These data suggest that IL-18 maturation by TAC activates AMPK and fatty acid metabolism, leading to adaptation to acute pressure overload.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report
  • Research Products

    (4 results)

All 2015 2014 Other

All Presentation (3 results) Remarks (1 results)

  • [Presentation] Interleukin-18 is Necessary to maintain mitochondriak function in pressure overload2015

    • Author(s)
      Iwasaku T, Hirotani S, et al
    • Organizer
      日本循環器学会
    • Place of Presentation
      Osaka, Japan
    • Year and Date
      2015-04-24 – 2015-04-26
    • Related Report
      2014 Research-status Report
  • [Presentation] Interleukin-18 Enhances Mitochondrial Function in Pressure Overload through AMP-activated Protein Kinase Activation2014

    • Author(s)
      Iwasaku T, Hirotani S, et al
    • Organizer
      American Heart Association
    • Place of Presentation
      Chicago, USA
    • Year and Date
      2014-11-15 – 2014-11-19
    • Related Report
      2014 Research-status Report
  • [Presentation] Low-dose Interleukin-18 is Necessary to maintain mitochondriak function in pressure overload2014

    • Author(s)
      Iwasaku T, Hirotani S, et al
    • Organizer
      American Heart Association BCVS
    • Place of Presentation
      Las Vegas, USA
    • Year and Date
      2014-07-14 – 2014-07-17
    • Related Report
      2014 Research-status Report
  • [Remarks] 兵庫医科大学 業績集 内科学 循環器内科

    • URL

      http://gyoseki-hyogoika.jp/hcmhp/KgApp?courc=3060010100&year=2014

    • Related Report
      2014 Research-status Report

URL: 

Published: 2014-04-04   Modified: 2018-03-22  

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