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Remodeling of cell-cell and cell-extracellular matrix communications during tissue injury

Remodeling of cell-cell and cell-extracellular matrix communications during tissue injury
组织损伤期间细胞与细胞和细胞与细胞外基质通讯的重塑
批准号:
12670214
负责人:
OYAMADA Masahito
金额:
$2.18万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2000
资助国家:
日本
项目状态:
已结题
起止时间:
2000 至 2001

项目摘要

项目成果

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中文摘要
翻译
大鼠心肌梗死边缘区细胞-细胞及细胞-细胞外基质相互作用的重塑我们在大鼠实验性心肌梗死模型上,用免疫共聚焦显微镜对心肌梗死边缘区缝隙连接(connexin 43)、桥粒(desmoplakin)、粘附连接(cadherin)和整合素(β1-integrin)的定位进行了三维分析。心肌梗死后间隙连接、桥粒和粘附连接的分布变化呈现相似但不一致的趋势。在早期阶段,缝隙连接几乎消失在树桩(心肌细胞的纵向边缘面对梗死),虽然桥粒和粘附连接减少,他们仍然存在。在愈合阶段,在残端,connexin 43,桥粒斑蛋白和钙粘蛋白之间的多个细胞过程起源于一个单一的心肌细胞密切相关。(在乳头状肌腱连接样结构形成过程中,细胞突起处β1-整合素增加。缝隙连接蛋白43的异常定位常伴有桥粒斑蛋白和钙粘蛋白在存活心肌细胞的侧面。这些结果表明,间隙连接分布的重塑与桥粒和粘附连接的变化密切相关,细胞内连接复合物的暂时形成是心肌梗死后细胞-细胞和细胞-细胞外基质相互作用重塑的一个因素。影像学显示结扎后早期(2-4小时)边界区心肌细胞内频繁的Ca^2+波。提示心肌梗死边缘区缝隙连接表达和功能异常可能与Ca^<2+>波有关。
英文摘要
Remodeling of cell-cell and cell-extra cellular matrix interactions at the border zone of rat myocardial infarctsWe conducted experimental infarction in rats and performed three-dimensional analysis of the localization of gap junctions (connexin43), desmosomes (desmoplakin), adherents junctions (cadherin) and integrins (β1-integrin) by immunoconfocal microscopy. After myocardial infarction, changes in the distribution of gap junctions, desmosomes and adherens junctions showed a similar but nonidentical tendency. In the early phase, gap junctions almost disappeared at stumps (longitudinal edges of cardiomyocytes facing the infarct), and, although desmosomes and adherents junctions decreased, they still remained. In the healing phase, at stumps, connexin43, desmoplakin and cadherin were closely associated between multiple cell processes originating from a single cardiomyocyte. (β1-Integrin at the cell process increased during the formation of papillary myotendinous junction-like structures. Abnormal localization of connexin43 was often accompanied by desmoplakin and cadherin on lateral surfaces of surviving cardiomyocytes. These findings suggested that remodeling of gap junction distribution was closely linked to changes in desmosomes and adherents junctions, and that temporary formation of intracellular junctional complexes was an element of the remodeling of cell-cell and cell-extra cellular matrix interactions after myocardial infarction.Abnormalities in intracellular calcium dynamics in cardiomyocytes at the border zone of rat myocardial infarctsReal time confocal Ca^<2+> imaging showed frequent Ca^<2+> waves in cardiomyocytes at border zones at early phases postligation (2-4 hours). These results suggest that abnormal expression and function of gap junctions could be associated with Ca^<2+> waves at the border zone of myocardial infarcts.
期刊论文(44)
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会议论文
Oyamada M et al.: "In vitro cardiomyocytic differentiation of mouse embryonic stem cells deficient in gap junction protein connexin43"Cardiac and Vascular Regeneration. 1. 54-64 (2000)
Oyamada M 等人:“间隙连接蛋白 connexin43 缺陷的小鼠胚胎干细胞的体外心肌细胞分化”心脏和血管再生。
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通讯作者:
Kaneko T, Oyamada M. et al.: "Three distinct types of Ca2+ waves in Langendorff-perfused rat heart revealed by real-time confocal microscopy"Circ. Res.. 86. 1093-1099 (2000)
Kaneko T、Oyamada M. 等人:“实时共聚焦显微镜揭示了 Langendorff 灌注大鼠心脏中三种不同类型的 Ca2 波”Circ。
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通讯作者:
Kaneko T,Tanaka H et al.: "Three distinct types of Ca2+ waves in langendorff-perfused rat heart revealed by real-time confocal microscopy"Circ Res. 86・10. 1093-1099 (2000)
Kaneko T、Tanaka H 等人:“通过实时共聚焦显微镜揭示 langendorff 灌注大鼠心脏中的三种不同类型的 Ca2+ 波”Circ Res 86・1099 (2000)。
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通讯作者:
小山田正人 他: "ギャップ結合細胞間コミュニケーションの機能異常と病態の発生"病理と臨床. 19・1. 67-72 (2001)
小山田正人等:“间隙连接细胞间通讯功能障碍和病理发展”病理学和临床研究19・1(2001)。
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共 44 条
    Epigenetic regulation of placental function by maternal nutrition as a mechanism of disease in DOHaD
    • 批准号:
      23617021
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $3.58万
    • 财政年份:
      2011
    • 负责人:
      OYAMADA Masahito
    • 依托单位:
    Studies on cell death and survival signals via connexin channels during cell injury
    • 批准号:
      17390118
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
      $9.42万
    • 财政年份:
      2005
    • 负责人:
      OYAMADA Masahito
    • 依托单位:
    Studies on gap-junctional intercellular communication as a mechanism regulating cell death in the cell society
    • 批准号:
      15390129
    • 项目类别:
      Grant-in-Aid for Scientific Research (B)
    • 资助金额:
      $7.04万
    • 财政年份:
      2003
    • 负责人:
      OYAMADA Masahito
    • 依托单位:
    Real-time and simulataneous analysis of gap junctional structure and function in living cells
    • 批准号:
      10670214
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.11万
    • 财政年份:
      1998
    • 负责人:
      OYAMADA Masahito
    • 依托单位:
    海外基金