Background: E(epithelial)-cadherin is a vital cell adhesion protein that plays a critical role in morphogenesis. Previous studies of E-cadherin distribution in human embryos have produced equivocal results.
Methods: Immunocytochemistry in conjunction with laser scanning confocal microscopy was used to detect E-cadherin in 97 human cleavage stage embryos and 35 blastocysts from normal and abnormal fertilization. An antibody against human placental E-cadherin was used to locate the protein.
Results: In blastomeres of cleaving embryos on the second and third days following insemination, E-cadherin was located in the cytoplasm--mostly concentrated in the cell margins. On the fourth day of development, the protein was relocated in compacting embryos to membranes in areas of cell-cell contact. In other abnormally compacted or non-compacted embryos with extensive cytoplasmic fragmentation, cell arrest or blastomere multi-nucleation, E-cadherin relocalization was either absent or erratic. In apparently normal blastocysts, E-cadherin in the inner cells was diffuse and cytoplasmic while properly organized trophectoderm cells were surrounded by a band of membrane E-cadherin. Disorganization of trophectoderm was associated with disruption of the regular E-cadherin banding pattern.
Conclusion: As in other mammalian species examined, E-cadherin distribution in human embryos is stage-dependent. Disturbances in the distribution of E-cadherin occur in embryos with cleavage abnormalities and suggest one path to abortive or abnormal blastulation and loss of embryonic viability. The implications of similar changes in the blastocyst are well worth investigating since they could threaten blastocyst integrity.