Fujio Y, Yamada-Honda F, Sato N, Funai H, Wada A, Awata N, Shibata N
Center for Adult Diseases, Osaka, Japan.
Cardiovasc Res. 1995 Dec;30(6):899-904.
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.
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.
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 subsarcolemmal 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.
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.
心肌细胞排列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是一种扩张型心肌病模型，表现出心肌细胞排列紊乱。本研究的目的是从细胞间黏附系统的角度分析Bio 14.6中细胞排列的紊乱情况。
将心肌病仓鼠Bio 14.6用作扩张型心肌病模型。通过光学显微镜和电子显微镜进行组织学研究。用抗A-CAM抗体通过免疫荧光显微镜和免疫印迹分析黏着连接特异性细胞黏附分子（A-CAM）的紊乱情况。
苏木精-伊红染色显示，与正常心肌相比，心肌病中闰盘的辨识度较低。电子显微镜显示，与正常仓鼠相比，Bio 14.6中闰盘处肌膜下电子密度降低，心肌细胞相互黏附减少。我们通过免疫荧光显微镜检查了心脏中A-CAM分子的定位。与正常心脏样本相比，Bio 14.6仓鼠中的荧光强度较弱且界限不清。我们测量了心脏中A-CAM的含量。在Bio 14.6仓鼠中，A-CAM的含量为正常成年仓鼠测量值的60±11%。新生仓鼠中A-CAM的降低程度较小（81±12%）。
在Bio 14.6仓鼠中，心脏组织学检查发现闰盘存在结构紊乱。生化分析表明，在闰盘区域细胞间黏附中起作用的A-CAM显著减少。这些结果表明，心肌病可能伴有闰盘区域细胞间黏附的结构破坏，这可能导致心肌细胞排列紊乱的病理特征。
