dc.description.abstract |
Epithelial–mesenchymal transition (EMT) is characterized by the loss of epithelial and acquisition of mesenchymal cell characteristics.
Our aim was to assess the epithelial phenotype in the pathogenesis of endometriosis with epithelial and mesenchymal
markers. We used 2 structural (keratin-18, -19 [K18, K19]), 1 membrane-associated (mucin-1 [MUC1]), and 2 mesenchymal
proteins (vimentin; zinc finger E-box-binding homeobox 1, [ZEB1]) to compare epithelial and mesenchymal characteristics in
eutopic endometrium with the 3 endometriotic entities, peritoneal, ovarian, and deep infiltrating endometriosis (DIE). Quantitation
showed no differences for K18, K19, and MUC1 between endometrium with and without endometriosis. Also, K18 was
not different between endometrium and endometriotic lesions. In contrast, K19 and MUC1 were modestly but significantly
decreased in the endometriotic lesions compared to endometrium. However, the maintained expression of epithelial markers in
all investigated tissues, regardless of the pathological condition, clearly indicates no loss of the epithelial phenotype. This is further
supported by the reduced presence of epithelial vimentin in endometriotic lesions which is in contrast to an increase in stromal
vimentin in ectopic endometrium, especially in ovarian endometriosis. The ZEB1 increase in endometriotic lesions, especially in
DIE, on the other hand suggests a role of partial EMT in the development of endometriotic lesions, possibly connected with the
gain of invasive capabilities or stemness. Taken together, although we found some hints for at least a partial EMT, we did not
observe a severe loss of the epithelial cell phenotype. Thus, we propose that EMT is not a main factor in the pathogenesis of
endometriosis. |
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