Disruption of cell-cell adhesion in an inbred strain of hereditary cardiomyopathic hamster (bio 14.6)
Disruption of cell-cell adhesion in an inbred strain of hereditary cardiomyopathic hamster (bio 14.6)
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DOI：
10.1016/0008-6363(95)00134-4
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发表时间：
1995-12-01
影响因子：
10.8
通讯作者：
Shibata, N
中科院分区：
文献类型：
--
作者：
Fujio, Y;YamadaHonda, F;Shibata, N
目的：心肌细胞紊乱是扩张型心肌病的病理特征。遗传性心肌病仓鼠Bio 14.6是扩张型心肌病模型，心肌细胞排列紊乱。本研究的目的是从生物14.6中细胞-细胞粘附系统的角度分析细胞排列的干扰。方法：采用Bio 14.6型心肌病仓鼠作为扩张型心肌病模型。光镜和电镜下进行组织学观察。采用免疫荧光显微镜和抗A-CAM抗体免疫印迹法分析了粘附体连接特异性细胞粘附分子（A-CAM）的紊乱情况。结果：苏木精-伊红染色显示，与正常心肌相比，心肌病的嵌盘不太清楚。电镜观察发现，与正常仓鼠相比，在Bio 14.6中心肌细胞相互粘附，嵌入盘肌束下电子密度降低。我们用免疫荧光显微镜检查了A-CAM分子在心脏中的定位。与正常心脏样品相比，Bio 14.6仓鼠的荧光强度较弱，界限不清。我们测量了心脏中A-CAM的含量。在Bio 14.6仓鼠中，A-CAM含量为正常成年仓鼠的60 +/- 11%。新生仓鼠的a - cam降低程度较小（81±12%）。结论：在Bio 14.6仓鼠心脏组织学检查中发现嵌盘结构紊乱。在生物化学上，在插盘区细胞间粘附中起作用的a - cam显著降低。这些结果表明，心肌病可能伴随着嵌盘区细胞-细胞粘附的结构破坏，这可能导致心肌细胞紊乱的病理特征。
Objective: Disarrangement of cardiomyocytes is a pathological characteristic of dilated cardiomyopathy. Hereditary cardiomyopathic hamster Bio 14.6, a model of dilated cardiomyopathy, displays disorder of cardiomyocyte arrangement. The aim of this study was to analyse the disturbance of cell alignment from the point of view of the cell-cell adhesion system in Bio 14.6. Method: Cardiomyopathic hamster Bio 14.6 was used as a model of dilated cardiomyopathy. Histological study was performed by light and electron microscopy. Disorder of the adherens junction-specific cell-adhesion molecule (A-CAM) was analysed by immunofluorescent microscopy and immunoblotting with anti-A-CAM antibody. Results: Hematoxylin-eosin staining revealed that intercalated disks were identifiable less clearly in cardiomyopathy than in a normal cardiac muscle. It was disclosed by electron microscopy that cardiomyocytes adhered to each other with reduction in subsarcoleminal electron density at intercalated disks in Bio 14.6 compared with normal hamsters. We examined the localization of the A-CAM molecule in heart by immunofluorescent microscopy. In contrast to normal cardiac samples, fluorescence was weak in intensity and unclearly demarcated in the Bio 14.6 hamsters. We measured the content of A-CAM in the heart. In Bio 14.6 hamsters, the content of A-CAM was 60 +/- 11% of that measured in normal adult hamsters. A-CAM was reduced to a lesser extent (81 +/- 12%) in the newborn hamsters. Conclusions: In Bio 14.6 hamster, structural disturbance of the intercalated disks was found on histological examination of the heart. Biochemically, A-CAM, which plays a role in intercellular adhesion in intercalated disk areas, decreased significantly. These results suggest that cardiomyopathy may be accompanied by structural disruption of cell-cell adhesion in intercalated disk regions, which may lead to the pathological feature of disarranged cardiomyocytes.