Abstract:
An epithelial-mesenchymal transition (EMT) is a biologic process that allows a polarized epithelial
cell, which normally interacts with basement membrane via its basal surface, to undergo multiple
biochemical changes that enable it to assume a mesenchymal cell phenotype, which includes
enhanced migratory capacity, invasiveness, elevated resistance to apoptosis, and greatly increased
production of ECM components. The aim of this study was to assess the epithelial phenotype in
the pathogenesis of endometriosis by performing IHC studies with epithelial and mesenchymal
markers. Researchers compared endometrium with and without endometriosis to peritoneal,
ovarian and deep infiltrating endometriosis (DIE) with two structural (keratin-18, -19), one
membrane-associated(mucin-1) and one mesenchymal protein (vimentin) to analyse the epithelial
and mesenchymal phenotype of the endometrial glands and endometriotic lesions.Quantitation
with the HSCORE showed no differences for keratin-18 (K18), keratin- 19 (K19) and mucin-1
(MUC1) between endometrium with and without endometriosis. Also, K18 was not different
between endometrium and endometriotic lesions. In contrast, K19 and MUC1 were significantly
decreased in the endometriotic lesions compared to endometrium. However, all three proteins were
found in almost every endometrial and endometriotic gland or cyst and in nearly all epithelial
cells. The study also established that protein expression of vimentin was lower in the endometriotic
lesions compared to the endometrium, especially in the ovary. The protein expression of the
epithelial markers in nearly all glands as well as in nearly all epithelial cells in the endometrium
endometriotic entities clearly indicates no loss of the epithelial cell phenotype. Additionally, the
reduced expression of vimentin in the endometriotic lesions, suggests no shift of the epithelial
phenotype to amesenchymal one. Thus, the study propose, that EMT is not a main factor in the
pathogenesis of endometriosis.
