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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

基本信息

批准号：
12670214
负责人：
OYAMADA Masahito
金额：
$ 2.18万
依托单位：
Kyoto Prefectural University of Medicine
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
起止时间：
2000 至 2001
项目状态：
已结题

项目摘要

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.

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。