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Regulatory mechanism to avoid or induce apoptosis in lymphocytes by AMP-activated protein kinase

Research Project

Project/Area Number 15591978
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Functional basic dentistry
Research InstitutionTokyo Dental College

Principal Investigator

KIZAKI Harutoshi  Tokyo Dental College, Department of Dentistry, professor, 歯学部, 教授 (60051653)

Co-Investigator(Kenkyū-buntansha) OHTA Kazumasa  Tokyo Dental College, Department of Dentistry, Instructor, 歯学部, 助手 (30307376)
YAMAMOTO Yasuhito  Tokyo Dental College, Department of Dentistry, Instructor, 歯学部, 助手 (80200848)
Project Period (FY) 2003 – 2005
Project Status Completed (Fiscal Year 2005)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2004: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2003: ¥2,200,000 (Direct Cost: ¥2,200,000)
KeywordsAMP-activated protein kinase / apoptosis / lymphocyte / glucocorticoid / thymus atrophy / masseter muscle / protein kinase C / starvation / 胸腺細胞 / 筋萎縮 / 低血糖 / Bcl-2ファミリー / AMP活性化キナーゼ / ストレス / 細胞生存シグナル / 細胞生存 / MAPキナーゼ
Research Abstract

T lymphocyte dynamics in inflammatory lesions are regulated by proliferation and apoptosis of the cells under various stresses. To elucidate the molecular mechanisms to avoid or induce apoptosis under stresses in T lymphocyte, the role of AMP-activated protein kinase (AMPK) was investigated in murine thymocytes and masseter muscle under various stress conditions. AMPK is known to be an enzyme activated by AMP and acting as a metabolic master switch capable of mediating the cellular adaptation to various stresses, and is a heterotrimeric complex consisting of a catalytic α and regulatory (β,γ) subunits. Each subunit has 2-3 isoforms. The present study showed that the cellular contents of the subunits and their isoform were different among tissues, suggesting different functions and regulation of AMPK activity in tissues. Starvation stress induced atrophy of thymus and masseter muscle associated with apoptosis. The main isoforms in thymus and masseter muscle induced by starvation stress which induced apoptosis in part by a stress hormone glucocorticoid.
Activation of AMPK by AICAR inhibited thymocyte apoptosis induced by various stimuli including glucocorticoid. Inhibition of apoptosis by AICAR was enhanced by activating protein kinase C, suggesting the interaction between AMPK and PKC pathways. Activation-induced cell death (AICD) plays a critical role in the homeostasis of T lymphocytes and Fas ligand (FasL) expression was involved in AICD. Expression of FasL following TCR stimulation was inhibited by proteasome inhibitors through blocking ERK activation as well as by activating AMPK.
These results suggest that AMPK has an important role to induce or avoid apoptosis under various stresses.

Report

(4 results)
  • 2005 Annual Research Report   Final Research Report Summary
  • 2004 Annual Research Report
  • 2003 Annual Research Report
  • Research Products

    (10 results)

All 2005 2004 Other

All Journal Article (8 results) Publications (2 results)

  • [Journal Article] Lidocain induced apoptosis and necrosis in U937 cells depending on its dosage2005

    • Author(s)
      Kamiya Y, Ohta K, Kaneko Y
    • Journal Title

      Biocmed Res 26-6

      Pages: 231-239

    • NAID

      130004903693

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Lidocain induced apoptosis and necrosis in U937 cells depending on its dosage2005

    • Author(s)
      Kamiya Y, Ohta K, Kaneko Y.
    • Journal Title

      Biocmed Res 26(6)

      Pages: 231-239

    • NAID

      130004903693

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Lidocain induced apoptosis and necrosis in U937 cells depending on its dosage2005

    • Author(s)
      Kamiya Y, Ohta K, Kaneko Y
    • Journal Title

      Biocmed Res 26(6)

      Pages: 231-239

    • NAID

      130004903693

    • Related Report
      2005 Annual Research Report
  • [Journal Article] Achacin induces cell death in Hela cells through two different mechanisms2004

    • Author(s)
      Kanzawa N, Shintani, S, Ohta K, Kitamima E, Kizaki H., Tsuchiya T
    • Journal Title

      Arch Biochem Biophys 422・1

      Pages: 103-109

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Modulation of thymocyte apoptosis by geldanamycin, a heat-shock protein 90-binding agent and 12-ο-tetradecanoyl-phorbol-13-acetate2004

    • Author(s)
      Ohta K, Wakabayashi M, Okoshi, R, Kizaki, H.
    • Journal Title

      Bull Tokyo Dental College 45-1

      Pages: 1-8

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Achacin induces cell death in Hela cells through two different mechanisms2004

    • Author(s)
      Kanzawa N, Shintani S, Ohta K, Kitamima E, Kizaki H., Tsuchiya T
    • Journal Title

      Arch Biochem Biophys 422(1)

      Pages: 1003-1009

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] Modulation of thymocyte apoptosis by geldanamycin, a heat-shock protein 90-binding agent and 12-O-tetradecanoyl-phorbol-13-acetate2004

    • Author(s)
      Ohta K, Wakabayashi M, Okoshi, R, Kizaki, H.
    • Journal Title

      Bull Tokyo Dental College 45(1)

      Pages: 1-8

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2005 Final Research Report Summary
  • [Journal Article] AICARによるリンパ球アポトーシスの回避機構2004

    • Author(s)
      太田一正, 大越林太郎, 佐藤裕, 木崎治俊
    • Journal Title

      痛風と核酸代謝 28(1)

      Pages: 66-66

    • NAID

      10014068631

    • Related Report
      2004 Annual Research Report
  • [Publications] Kanzawa N, Shintani, S, Ohta K, Kitamima E, Kizaki H., Tsuchiya T: "Achacin induces cell death in Hela cells through two different mechanisms"Archives of Biochemistry and Biophysics. 422. 103-109 (2004)

    • Related Report
      2003 Annual Research Report
  • [Publications] Ohta K, Wakabayashi M, Okoshi, R, Kizaki, H.: "Modulation of thymocyte apoptosis by geldanamycin, a heat-shock protein 90-binding agent and 12-O-tetradecanoyl-phorbol-13-acetate"Bulletin of Tokyo Dental College. 45(1)(In press). (2004)

    • Related Report
      2003 Annual Research Report

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Published: 2003-04-01   Modified: 2016-04-21  

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