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From the Department of Pathology,*
Leiden University
Medical Center, Leiden; and the Department of Obstetrics and
Gynecology,
Academic Hospital Utrecht,
Utrecht, The Netherlands
Uterine cervix represents a convenient model for the study of the
gradual transformation of normal squamous epithelium via low- to
high-grade squamous intraepithelial lesions (SILs). Because
SIL, on the basis of the cytokeratins expressed, are
thought to originate from the reserve cells, we analyzed
whether SILs also show a reserve cell phenotype with respect to
intercellular interactions. The changes in expression and subcellular
localization of the components of the adherens junction and desmosomal
complexes were investigated in normal, metaplastic, and
premalignant cervical epithelium, as well as in cell cultures
derived from these tissues. The results suggest that 1) during
progression of SILs, E-cadherin is suppressed, with its
role in cell-cell connections diminishing; 2) P-cadherin, in
contrast, becomes the predominant cadherin in high-grade SILs;
3) the level of cellular 
-catenin is dramatically decreased in
high-grade SILs; 4) the level of ß-catenin is decreased during
progression of SILs, with plakoglobin suggestively becoming the
predominant catenin mediating connection of cadherins to the
cytoskeleton; 5) the assembly of desmosomes is affected during
progression of SILs and is accompanied by a dramatically decreased
expression for desmogleins and desmoplakins (I, II); and 6)
expression of differentiation markers (involucrin, CK13) in
high-grade SILs seems to be controlled by P-cadherin as opposed to
E-cadherin in the normal tissue counterpart. We conclude that during
development of cervical lesions substantial (both quantitative and
qualitative) changes occur in cell-cell junctions, making the
interactions of cells in lesions dissimilar from those of reserve
cells, basal cells, or cells of immature squamous
metaplasia, despite existing morphological similarity between
all of these cell types and cells of high-grade lesions.
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