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Introduction
Endometrial receptivity plays a key role in the establishment of a successful implantation and its impairment may contribute to infertility in women (1). A variety of molecules such as hormones, receptors, adhesion molecules, growth factors and cytokines mediate the embryomaternal crosstalk and facilitate the reception of a blastocyst and the establishment of implantation (2). During the menstrual cycle uterine receptivity is regulated by the secretion of the ovarian steroids. Endometrial proliferation is induced by estrogen during the preovulatory phase, whereas progesterone causes secretory changes in the estrogen- primed endometrium (3).
Ligand-specific intracellular receptors located in stro. mal and epithelial endometrial cells mediate the actions of estrogen and progesterone (4). It is thought that the pres. ence of progesterone after appropriate estrogen priming is required to stimulate key implantation-specific events in the mid-secretory phase of the menstrual cycle (5).
Estrogen receptor-alpha ( ER-α ) increases during the proliferative phase in response to estrogen and is downregulated during the window of implantation in response to progesterone (6). The disappearance of ER-α at the time of implantation has been reported in most mammalian species (7). The decline in ER-α coincides with endometrial gene expression in the mid-luteal phase, and is a critical event in the establishment of endometrial receptivity (8). High levels of ER-α during implantation were observed in women with polycystic ovarian syndrome (PCOS) and endometriosis. Elevated expression of ER-α in both groups of patients was associated with the reduction in beta 3 integrin expression, a marker of endometrial receptivity (9). It has been suggested that the disappearance of ER-α at the time of implantation may disturb the expression pattern of proteins that regulate the endometrial receptivity.
Glycodelin-A ( GdA ) is a progesterone-regulated glycoprotein with immunosuppressive properties that is highly upregulated in glandular epithelium at implantation and plays a role in the formation a receptive endometrium (10). GdA expression is concurrent with pinopode formation in the receptive endometrium (11), indicating that it can potentially be seen as a diagnostic marker of morphological differentiation of human endometrium (12). A lower glycodelin expression in secretory phase was found in eutopic endometrium of endometriosis patients and in uterine flushings from women with unexplained infertility when compared to the healthy controls (13, 14).
Assuming that unexplained infertility can be...