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Apoptosis in the conduction system of the heart in the senscence accelerated mouse (SAM)

Research Project

Project/Area Number 07670820
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Circulatory organs internal medicine
Research InstitutionOsaka Medical College

Principal Investigator

TERASAKI Fumio  Osaka Medical College, The Third Dovision of Internal Medicine, Assistant Professor, 医学部, 助手 (20236988)

Project Period (FY) 1995 – 1996
Project Status Completed (Fiscal Year 1996)
Budget Amount *help
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1996: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1995: ¥1,800,000 (Direct Cost: ¥1,800,000)
Keywordssenscence accelerated mouse / cardiac conduction system / apoptosis / ultrastructure / aging / 老化促進マウス
Research Abstract

*Background and Purpose* Cardiac disorders such as heart block often develop in aged patients, but the pathogenesis remains unexplained. The senescence accelerated mouse (SAM) is a novel murine model of accelerated senescence. To clarify loss of cardiocytes in the conduction system of aging heart, atrioventricular (AV) conducting tissue from SAM was examined with conventional light (LM) and transmission electron microscopy (EM). Both of light ane electron microscopic in situnick end labeling of dUTP (TUNEL) was also applied. *Results* LM showed atrophic myocardial cells with shrunk nuclei occasionally but not very often. EM revealed that cardiocytes sporadically underwent a variety of degenerative processes, which were characterized by disorganization of myofibrils and intermediate filaments, enlarged sarcoplasmic reticulum, intracytoplasmic vacuoles, curvilinear membranous formation, and rare disruptions of the plasma membrane. Nuclear chromatin was condensed and marginated beneath apparently preserved nuclear membrane in some degenerated cardiocytes. In the interstitium, some macrophages appeared to have phagocytosed degenerated cardiocytes and included some residual bodies, but there was no infiltration of inflammatory cells. Cardiocytes degenerated more often in AV conducting tissue than in working myocardium. Furthermore, light and electron microscopic TUNEL-positive cardiocytes were seen occasionally in AV conducting tissu. *Conclusion* It is concluded that myocardial cell death in AV conduction system of SAM hearts may be induced by apoptosis which is programd in aging process of conducting cardiocytes.

Report

(3 results)
  • 1996 Annual Research Report   Final Research Report Summary
  • 1995 Annual Research Report
  • Research Products

    (5 results)

All Other

All Publications (5 results)

  • [Publications] 下村裕章: "老化促進モデルマウス(SAM)の心臓刺激伝導系における微細構造病変" 心筋の構造と代謝. 18. 189-193 (1996)

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] Hiroaki Shimomura, Fumio Terasaki, Makoto Okabe, Tetuya Hayashi, Kei-ichi Higuchi, Masanori Hosokawa, Keishiro Kawamura: "Ultrastructural alterations of the cardiac conduction system in the senescence accelerated mouse (SAM)" Cardiac Structure and Metabolism. Volume 18. 189-193 (1996)

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      1996 Final Research Report Summary
  • [Publications] 下村裕章: "老化促進モデルマウス(SAM)の心臓刺激伝導系における微細構造病変" 心筋の構造と代謝. 18. 189-193 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] Hiroaki Shimomura: "Ultrastructural Remodelling in the Heart with Special Reference to Myocardial Cell Death in the Senescence Accelerated mouse (SAM)" Japanese Circulation Journal. 60. 436-437 (1996)

    • Related Report
      1996 Annual Research Report
  • [Publications] 下村 裕章: "老化促進モデルマウス(SAM)の心臓刺激伝導系における微細構造病変" 心筋の構造と代謝. 18(予定). (1996)

    • Related Report
      1995 Annual Research Report

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Published: 1995-04-01   Modified: 2016-04-21  

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