Cell adhesion to the apical pole of epithelium: a function of cell polarity.
Human uterine epithelium displays a distinct polarized organization with apical, lateral, and basal plasma membrane domains. Although non-adhesive throughout most of the menstrual cycle, epithelial cells allow attachment of trophoblast cells to their apical pole during embryo implantation. A recent hypothesis postulates that epithelial cells turn off genes for apical-basal polarity and turn on genes for a more mesenchyme-like phenotype allowing cell-cell interaction with trophoblast. Using an in vitro assay human uterine cell lines (RL95-2, HEC-1-A, AN3-CA) were selected on the basis of adhesiveness for trophoblast-type cells (JAR). Subsequently, uterine cells were examined for epithelium-specific ultrastructure using transmission electron microscopy, and for the expression of E-cadherin, alpha 6-, beta 1-, beta 4-integrin subunits and cytokeratin using immunocytochemistry, confocal laser scanning microscopy, and surface replication technique. HEC-1-A monolayers are non-adhesive for JAR cells and appear highly polarized expressing E-cadherin, alpha 6-, beta 1-, beta 4-integrin subunits, and cytokeratin. Both, integrins and E-cadherin, are present at the lateral membrane. RL95-2 monolayers which are adhesive for JAR cells appear non-polarized. Like HEC-1-A cells, RL95-2 cells express E-cadherin, alpha 6-, beta 1-, and beta 4-integrin subunits, and cytokeratin. In contrast to HEC-1-A cells, integrins and E-cadherin are distributed at the entire cell surface. AN3-CA monolayers are non-adhesive for JAR cells and appear non-polarized. Cells lack epithelial-specific markers such as keratin and E-cadherin. They show only low expression of alpha 6-, beta 1-integrin subunits and lack beta 4-integrin subunit. Conversely, they express vimentin. Thus, modulation of the epithelial phenotype of uterine cells, i.e. loss of apical-basal polarity, might prepare the apical cell pole for cell-cell interaction with trophoblast. However, loss of cell polarity would not lead to enhancement of adhesiveness for trophoblast if accompanied by a loss of epithelium-specific adhesion molecules.
Thie
M
M
Institute of Anatomy, University of Essen, Medical School, Germany.
Harrach-Ruprecht
B
B
Sauer
H
H
Fuchs
P
P
Albers
A
A
Denker
H W
HW
D015820:Cadherins / Q000032:analysis; D002448:Cell Adhesion / Q000502:physiology*; D002462:Cell Membrane / Q000502:physiology; D016764:Cell Polarity / Q000502:physiology*; D004717:Endometrium / Q000166:cytology / Q000502:physiology*; D004847:Epithelial Cells; D004848:Epithelium / Q000502:physiology; D005260:Female; D006801:Humans; D016023:Integrins / Q000032:analysis; D010641:Phenotype; D014327:Trophoblasts / Q000166:cytology / Q000502:physiology*; D014407:Tumor Cells, Cultured
D015820:Cadherins; D016023:Integrins