Mast Cell Tryptase and Carboxypeptidase A3 in the Formation of Ovarian Endometrioid Cysts

Abstract

The mechanisms of ovarian endometrioid cyst formation, or cystic ovarian endometriosis, still remain to be elucidated. To address this issue, we analyzed the involvement of mast cell (MC) tryptase and carboxypeptidase A3 (CPA3) in the development of endometriomas. It was found that the formation of endometrioid cysts was accompanied by an increased MC population in the ovarian medulla, as well as by an MC appearance in the cortical substance. The formation of MC subpopulations was associated with endometrioma wall structures. An active, targeted secretion of tryptase and CPA3 to the epithelium of endometrioid cysts, immunocompetent cells, and the cells of the cytogenic ovarian stroma was detected. The identification of specific proteases in the cell nuclei of the ovarian local tissue microenvironment suggests new mechanisms for the regulatory effects of MCs. The cytoplasmic outgrowths of MCs propagate in the structures of the stroma over a considerable distance; they offer new potentials for MC effects on the structures of the ovarian-specific tissue microenvironment under pathological conditions. Our findings indicate the potential roles of MC tryptase and CPA3 in the development of ovarian endometriomas and infer new perspectives on their uses as pharmacological targets in personalized medicine.

Ovaries of estrogen receptor 1-deficient mice show iron overload and signs of aging

“…Mast cells are present in the ovary at all stages of rodent estrous cycle and human ovaries and can release various mediators such as tumor necrosis factor alpha (13,(67)(68)(69)(70). In addition, mast cells are involved in iron-induced conversion of macrophages to foam cells during hemorrhage (66).…”

Mast Cells in Human Health and Diseases 2.0

“…MCs release a plethora of factors involved variously in inflammation, pain, fibroblast proliferation, and angiogenesis—processes known to be involved, among other things, in the pathogenesis of endometriosis [ 21 , 22 ]. Evidence reports that MCs, under the influence of estrogen, are recruited to the endometriotic lesion microenvironment and play an active role in endometriosis pathophysiology [ 23 , 24 ].…”