Epithelial to Mesenchymal Transition (EMT) in the Pathogenesis of Endometriosis
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.