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A study on the mechanism of dedifferentiation and hypertrophy of vascular myocytes in atherosclerotic lesions

Research Project

Project/Area Number 13670695
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionThe University of Tokyo

Principal Investigator

SUZUKI Etsu  The University of Tokyo, Faculty of Medicine, Research Associate, 医学部附属病院, 助手 (40313134)

Co-Investigator(Kenkyū-buntansha) NAGATA Daisuke  The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
KAKOKI Masao  The University of Tokyo, Faculty of Medicine, Medical Staff, 医学部附属病院, 医員
HIRATA Yasunobu  The University of Tokyo, Faculty of Medicine, Lecturer, 医学部附属病院, 講師 (70167609)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2002: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Keywordsatherosclerosis / vascular myocytes / transcription factors
Research Abstract

We examined the roles of the transcription factors myocyte enhancer factor 2 (MEF2)- and nuclear factors of activated T cells (NFAT) in dedifferentiation and hypertrophy of vascular myocytes. Angiotensin II (ATII) induced the promoter activity of the nonmuscle-type myosin heavy chain B (NMMHCB) gene, which we used as a marker of the dedifferentiated state of VSMCs, and this increase was inhibited by calcineurin inhibitors, but not by the dominant negative mutants of MEF2A. Overexpression of a constitutively active calcineurin mutant stimulated the promoter activity of the NMMHCB gene. ATII increased protein synthesis and this increase was inhibited by infection with an adenovirus construct expressing the dominant nagative mutant of MEF2A, but not by calcineurin inhibitors. These results suggest that the MEF2- and calcineurin/NFAT-dependent pathways have distinct roles in vascular myocytes

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Suzuki E et al.: "Angiotensin II induces myocyte enhancer factor 2-and calcineurin/nuclear factor of activated T cell-dependent transcriptional activation in vascular myocytes"Circulation Research. 90. 1004-1011 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Suzuki E et al.: "Constitutive activation of proto-oncogene protein p21 induces cell cycle arrest in the G1 phase in contact-inhibited vascular endothelial cells"Hypertension Research. 25. 773-778 (2002)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Suzuki E et al.: "Angiotensin II induces myocyte enhancer factor 2- and calcineurin/nuclear factor of activated T cell-dependent transcriptional activation in vascular myocytes"Circ Res. 90. 1004-1011 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Suzuki E et al.: "Constitutive activation of proto-oncogene protein p21 induces cell cycle arrest in the G1 phase in contact-inhibited vascular endothelial cells"Hypertension Research. 25. 773-778 (2002)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Suzuki E et al.: "Angiotensin II induces myocyte enhancer factor 2-and calcineurin/nuclear factor of activated T cell-dependent transcriptional activation in vascular myocytes"Circulation Research. 90. 1004-1011 (2002)

    • Related Report
      2002 Annual Research Report
  • [Publications] Suzuki E et al.: "Constitutive activation of proto-oncogene protein p21 induces cell cycle arrest in the G1 phase in contact-inhibited vascular endothelial cells"Hypertension Research. 25. 773-778 (2002)

    • Related Report
      2002 Annual Research Report

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Published: 2001-04-01   Modified: 2016-04-21  

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