Cadherins in the human placenta – epithelial–mesenchymal transition (EMT) and placental development

Migration of extravillous trophoblasts into the maternal decidua-possible EMT? Villous cytotrophoblasts are bound together tightly and develop into proliferative cell columns prior to commencing migration as extravillous trophoblasts. Upon acquisition of this migratory ability, extravillous trophoblasts tend to lose their tight epithelial assembly and phenotype, becoming loosely attached, subsequently invading the maternal decidua as interstitial cytotrophoblasts. The process by which placental trophoblasts originate as epithelial cells and are subsequently triggered to change from a epithelial to a mesenchyme-like migratory phenotype, resembling epithelial-to-mesenchymal transition (EMT) identified in other developmental processes. Hence, this change in morphology is likely to involve changes in cadherin expression and function, as has been observed in all other EMTs.

Cell junctional complexes linking epithelial cells. The localisation of major cell junctional molecules in epithelial cells. Epithelial cells maintain their attachment and morphology through molecules located at the cytoskeleton, and cell–cell junctions. Gap junctions allow for cell–cell communication and interchange of molecules between cells. Tight junctions enable cells to form a barrier to uncontrolled molecular diffusion from one side of the cell sheet to the other. The structure of these adhesions is buttressed by adherens junctions linked via circumferential ring bundles of actin fibrils. Further adhesive stabilisation is via desmosomal junctions with intermediate filaments. The specific cell–cell link of these adherens and desmosomal junctions is via cadherins, and integration with the actin cytoskeleton involves β-catenin. Loss of these junctional components can lead to epithelial–mesenchymal transition (EMT).