Impaired down-regulation of E-cadherin and beta-catenin protein expression in endometrial epithelial cells in the mid-secretory endometrium of infertile patients with endometriosis

Abstract

Context: Only a few, small, human studies on E-cadherin and beta-catenin expression in normal cycling human endometrium have been reported. It remains unclear whether expression of these molecules might be altered in the endometrium of infertile patients with endometriosis.

Objectives: The aim of the present study was to investigate E-cadherin and beta-catenin expression in the endometrium of infertile patients with endometriosis, those with uterine fibromas, and patients with unexplained infertility.

Design: Expression levels of E-cadherin and beta-catenin mRNA and/or protein in the endometrium of infertile patients with endometriosis (n = 151), those with uterine fibromas (n = 41), patients with unexplained infertility (n = 9), as well as healthy fertile controls (n = 57) were measured. This study utilized laser capture microdissection, real-time RT-PCR, and immunohistochemistry.

Results: No significant differences in E-cadherin or beta-catenin mRNA expression in microdissected epithelial cells were observed among the different groups throughout the menstrual cycle. However, very low or no protein expression of E-cadherin, total beta-catenin, or dephosphorylated beta-catenin in luminal and glandular epithelial cells was detected in the mid-secretory endometrium of healthy fertile controls. E-cadherin, total beta-catenin, and dephosphorylated beta-catenin protein expression in the mid-secretory endometrium of infertile patients with endometriosis or unexplained infertility was significantly higher compared to that of healthy fertile controls in both luminal and glandular epithelial cells.

Conclusions: These findings suggest that impaired down-regulation of E-cadherin and beta-catenin protein expression, along with Wnt/beta-catenin signaling pathway activation during the window of implantation, might be one of the potential molecular mechanisms of infertility in patients with endometriosis.