Similar Characteristics of Endometrial and Endometriotic Epithelial Cells

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This study compared epithelial and mesenchymal markers in eutopic endometrium and endometriotic lesions, finding maintained epithelial phenotypes and suggesting partial EMT plays a role in endometriosis development.

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The study examined whether epithelial-mesenchymal transition (EMT) occurs in endometriosis by comparing epithelial and mesenchymal marker expression in eutopic endometrium versus three endometriotic entities: peritoneal, ovarian, and deep infiltrating endometriosis (DIE). Using markers keratin-18, keratin-19, MUC1, vimentin, and ZEB1, the authors found no differences in K18 between endometrium and lesions, and no differences for K18, K19, or MUC1 overall when eutopic endometrium was compared with endometriosis; however, K19 and MUC1 were modestly but significantly decreased in endometriotic lesions. They observed maintained epithelial marker expression overall, with reduced epithelial vimentin in endometriotic lesions (contrasting with reported increases in stromal vimentin) and increased ZEB1 especially in DIE, suggesting possible partial EMT. The paper concludes that EMT is not a main factor in endometriosis pathogenesis. This paper is centrally about endometriosis — it directly tests EMT-related epithelial versus mesenchymal phenotypes across eutopic endometrium and peritoneal, ovarian, and deep infiltrating endometriosis lesions.

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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). Quanti-tation 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. Similar content being viewed by others

References

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mesh:D004715

MeSH descriptors

Endometriosis Endometrium Epithelial Cells Endometriosis Endometriosis Endometrium Endometrium Epithelial Cells Epithelial Cells Epithelial-Mesenchymal Transition Female Humans Keratin-18 Keratin-18 Keratin-19 Keratin-19 Mesoderm Mesoderm Mucin-1 Mucin-1

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