Department of Perinatal Medicine, Pregnancy Research Centre, The Royal Women's Hospital, Flemington Road, Parkville 3052, Victoria, Australia.
Placenta. 2010 Sep;31(9):747-55. doi: 10.1016/j.placenta.2010.06.017. Epub 2010 Jul 24.
Colonisation of the maternal uterine wall by the trophoblast involves a series of alterations in the behaviour and morphology of trophoblast cells. Villous cytotrophoblast cells change from a well-organised coherently layered phenotype to one that is extravillous, acquiring a proliferative, migratory and invasive capacity, to facilitate fetal-maternal interaction. These changes are similar to those of other developmental processes falling under the umbrella of an epithelial-mesenchymal transition (EMT). Modulation of cell adhesion and cell polarity occurs through changes in cell-cell junctional molecules, such as the cadherins. The cadherins, particularly the classical cadherins (e.g. Epithelial-(E)-cadherin), and their link to adaptors called catenins at cell-cell contacts, are important for maintaining cell attachment and the layered phenotype of the villous cytotrophoblast. In contrast, reduced expression and re-organization of cadherins from these cell junctional regions promote a loosened connection between cells, coupled with reduced apico-basal polarity. Certain non-classical cadherins play an active role in cell migration processes. In addition to the classical cadherins, two other cadherins which have been reported in placental tissues are vascular endothelial (VE) cadherin and cadherin-11. Cadherin molecules are well placed to be key regulators of trophoblast cell behaviour, analogous to their role in other developmental EMTs. This review addresses cadherin expression and function in normal and diseased human placental tissues, especially in fetal growth restriction and pre-eclampsia where trophoblast invasion is reduced.
滋养层对母体子宫壁的殖民化涉及滋养层细胞行为和形态的一系列改变。绒毛滋养层细胞从组织有序的同质层状表型转变为绒毛外的表型，获得增殖、迁移和侵袭能力，以促进胎儿-母体相互作用。这些变化类似于其他发育过程，属于上皮-间充质转化（EMT）的范畴。细胞黏附与细胞极性的调节通过细胞-细胞连接分子的变化发生，如钙黏蛋白。钙黏蛋白，特别是经典钙黏蛋白（如上皮型（E）-钙黏蛋白），以及它们与细胞-细胞连接处称为连环蛋白的衔接子的联系，对于维持绒毛滋养层细胞的附着和层状表型很重要。相比之下，这些细胞连接区域钙黏蛋白的表达减少和重新组织促进了细胞之间连接的松动，同时伴随着顶端-基底极性的降低。某些非经典钙黏蛋白在细胞迁移过程中发挥积极作用。除了经典钙黏蛋白外，在胎盘组织中还报道了另外两种钙黏蛋白：血管内皮（VE）钙黏蛋白和钙黏蛋白-11。钙黏蛋白分子非常适合作为滋养层细胞行为的关键调节剂，类似于它们在其他发育 EMT 中的作用。这篇综述讨论了钙黏蛋白在正常和病变人类胎盘组织中的表达和功能，特别是在胎儿生长受限和子痫前期，其中滋养层浸润减少。
