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

感知加速小鼠（SAM）心脏传导系统的细胞凋亡

• 批准号: 07670820
• 负责人: TERASAKI Fumio
• 金额: $ 1.34万
• 依托单位: Osaka Medical College
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07670820/
• 关键词: senscence accelerated mouse; cardiac conduction system; apoptosis; ultrastructure; aging; 老化促進マウス

*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.

背景与目的心脏传导阻滞等心脏疾病常见于老年患者，但其发病机制尚不清楚。衰老加速小鼠(SAM)是一种新型的加速衰老的小鼠模型。为阐明衰老心脏传导系统中心肌细胞的丢失，对SAM房室传导组织进行常规光镜(LM)和透射电子显微镜(EM)观察。同时用光镜和电子显微镜对dUTP(TUNEL)进行Situnick末端标记。结果光镜下可见心肌细胞萎缩，核变小，但不常见。透射电子显微镜显示，心肌细胞零星地经历了各种退变过程，其特征是肌原纤维和中间丝结构紊乱，肌浆网增大，胞质内空泡形成，膜形成曲线状，质膜罕见破裂。在一些变性的心肌细胞中，核染色质在明显保存的核膜下凝集和边集。间质内可见部分巨噬细胞吞噬变性的心肌细胞，并有部分残存小体，但未见炎性细胞浸润。房室传导组织中的心肌细胞比工作心肌中的细胞更易变性。此外，光镜和电子显微镜下可见房室传导组织中偶见TUNEL阳性的心肌细胞。结论SAM心脏房室传导系统的心肌细胞死亡可能是由传导细胞衰老过程中的细胞凋亡引起的。

项目成果

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)

Hiroaki Shimomura：“心脏超微结构重塑，特别参考衰老加速小鼠（SAM）中的心肌细胞死亡”日本循环杂志。

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)

Hiroaki Shimomura：“加速衰老模型小鼠（SAM）心脏传导系统的超微结构损伤”心肌结构和代谢18（计划）。

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)

Hiroaki Shimomura：“加速衰老模型小鼠 (SAM) 心脏传导系统的超微结构损伤” 心肌结构和代谢。 18. 189-193 (1996)

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 Metabol

Hiroaki Shimomura、Fumio Terasaki、Makoto Okabe、Tetuya Hayashi、Kei-ichi Higuchi、Masanori Hosokawa、Keishiro Kawamura：“衰老加速小鼠 (SAM) 心脏传导系统的超微结构改变” 心脏结构和代谢