Immunophenotypic endometrium profile in experimental hyperplasia

Abstract

Aim. To study the topography and expression of cell cycle markers, as well as those of inflammation and immune response, by the method of immunohistochemistry using an experimental model of endometrial hyperplasia.Materials and methods. Endometrial hyperplasia was modeled in laboratory rats by ovariectomy and transdermal administration of estrogen to form hyperestrogenism. Morphological changes were verified by a histological method. The immunophenotypic profile was assessed by immunohistochemistry. The obtained digital values were processed by mathematical and statistical methods.Results. The modelled endometrial hyperplasia indicated an increase in the glandular component, a decrease in the expression of estrogen receptors in the uterine horns, an increase in the mitotic activity of epithelial cells in the uterine body, an activation of cell apoptosis in all its departments, as well as a decrease in the expression of plasmocyte markers (CD138) in the stroma of all parts of the uterus and T-lymphocytes (CD8) in the stroma the body of the uterus.Conclusion. Structural changes in endometrial hyperplasia in the setting of hyperestrogenism are caused by cell cycle dysregulation. At the same time, intracellular autoregulation systems are more effective in the uterine horns, with no changes being observed in the expression of estrogen receptors in the uterine body and the mitotic activity of cells being increased. Given the deficiency of immunocompetent T cells, the risk of tissue and cellular transformations increases in this area.