Menstruation is associated with disordered expression of desmoplakin I/II and cadherin/catenins and conversion of F- to G-actin in endometrial epithelium.

Endometrium is unique since it is the only tissue that undergoes regular cyclic bleedings. Menstrual shedding is associated with the breakdown of endometrium, including the fragmentation of endometrial glands. To gain insight into the underlying basis of fragmentation of the endometrial epithelium during the menstrual phase, we examined the expression of proteins implicated in epithelial cell-cell binding in human endometria throughout the entire menstrual cycle. Western blotting failed to reveal differences in the relative amount of E-cadherin, alpha- or beta-catenin or actin in the menstrual endometria compared with those in the proliferative or secretory phases. However, specific changes in the expression pattern of these proteins as well as desmoplakin I/II were detected by immunohistochemical staining in epithelial cells of menstrual endometria. Desmoplakin I/II, E-cadherin, alpha- and beta-catenins and beta-actin were localized to intercellular borders as well as the luminal and basal regions of glandular epithelium during the proliferative and secretory phases. Immunoreactivity of E-cadherin and alpha-catenin was confined to epithelial cells, whereas beta-catenin and beta-actin were present in epithelial cells, as well as in stroma and endothelial cells. Binding of F-actin to fluorescein isothiocyanate-labelled phalloidin localized this form of actin to the intercellular borders, and the basal and luminal cytoplasm of epithelial cells in proliferative and secretory endometria. Menstrual shedding was associated with disorganization of the site-specific distribution of desmoplakin I/II, E-cadherin and alpha- and beta-catenins.(ABSTRACT TRUNCATED AT 250 WORDS)