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首页> 外文期刊>Cell and Tissue Research >Ultrastructural changes in endometrial desmosomes of desmoglein 2 mutant mice
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Ultrastructural changes in endometrial desmosomes of desmoglein 2 mutant mice

机译：脱胶2突变小鼠子宫内膜脱落中的超微结构变化

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The intercellular binding of desmosomal junctions is mediated by cadherins of the desmoglein (Dsg) and desmocollin (Dsc) type. Dsg2 mutant mice with deletion of a substantial segment of the extracellular EC1-EC2 domain, which is believed to participate in homo- and heterophilic desmosomal cadherin interactions, develop cardiac fibrosis and ventricular dilation. Widening of the intercellular cleft and complete intercalated disc ruptures can be observed in the hearts of these mice. Since a reduced litter size of homozygous Dsg2 mutant mice was noted and a functional correlation between desmosomes and embryo implantation has been deduced from animal studies, we looked for an alteration of desmosomes in uterine endometrial epithelium. Shape and number of desmosomes as well as the expression of Dsg2 and the desmosomal plaque protein desmoplakin (Dsp) were investigated by electron microscopy and immunohistochemistry in 12 oestrous-dated mice (7 wildtype and 5 homozygous Dsg2 mutant mice) at the age of 9-17weeks. The immunohistochemical detection of Dsg2 was diminished in the mutants and the number of desmosomes was significantly reduced as revealed by electron microscopy. In addition, the intercellular desmosomal space measured in electron micrographs was considerably widened in the Dsg2 mutants. The increased intercellular spacing can be explained by the partial deletion of the extracellular EC1-EC2 domain of Dsg2. Whether these changes explain the reduced number of offspring of homozygous Dsg2 mutant mice remains to be further investigated.
机译：去染色结的间细胞间结合由脱果膜（DSG）和Desmocollin（DSC）类型的钙丝介导。 DSG2突变小鼠缺失细胞外EC1-EC2结构域的大量段，据信均可参与同源和脱髓鞘钙粘蛋白相互作用，发育心肌纤维化和心室扩张。在这些小鼠的心中可以观察到细胞间裂隙和完全插入的椎间盘突裂的加宽。由于注意到纯合DSG2突变小鼠的降低的凋落物尺寸，并且从动物研究中推导出脱皮和胚胎植入之间的功能相关性，因此我们寻找子宫子宫内膜上皮中的脱染料的改变。通过电子显微镜和免疫组织化学在12岁 - 17周。在突变体中减少DSG2的免疫组织化学检测，并且如电子显微镜透露的那样显着降低DESmosomes的数量。此外，在电子显微照片中测量的细胞间脱染型空间在DSG2突变体中显着加宽。通过DSG2的细胞外EC1-EC2结构域的部分缺失可以解释增加的细胞间距。这些变化是否解释了纯合DSG2突变小鼠的减少数量的后代仍然进一步研究。

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