HLA-G and endometrial receptivity.

Abstract

The endometrium is a complex and dynamic tissue, which experiences physiological and cyclical changes each month, in response to ovarian hormones, cytokines and chemokines [1-3]. The embryo is capable of attach to the uterine endometrium during a short and selflimited period, in which the endometrial tissue acquires a functional condition that allows the interaction trophoblast-endometrium and therefore, it is receptive. The embryo enters the uterine cavity as an unhatched blastocyst and undergoes its final development through hatching to attachment to the uterine luminal epithelium within the environment of uterine fluid. The embryo first enters the uterine cavity as blastocyst and attached to the uterine epithelium [4] (Figure 1). Decidualization of endometrial stromal cells is mainly induced by ovarian steroids and progesterone-dependent decidualization is mediated in part by the second messenger cAMP [5], decidualization is taking place with the secretory transformation of the uterine glands, particularly of specialized uterine natural killer cells and vascular remodelling [6]. Endometrial receptivity (ER) is defined as a temporary unique factors sequence that make the endometrium receptive to the embryonic implantation [7]. This specific period is regulated by a combination of ovarian steroids hormones and genetic factors and is known as “window of implantation” (WOI). It takes place between 6 and 10 days after ovulation [8], and it remains receptive during a short period of time, about the 20-24th of a cycle of 28 days [9]. During this period the endometrium undergoes morphological, cytoskeletal, biochemical, and genetic changes to become functionally competent [10]. Embryo implantation is a process comprising several cellular, ultrastructural and molecular mechanisms initiated and mediated by the endometrium, the embryo and the interaction of both. In order that the embryonic implantation takes place, there is indispensable the concurrence of three fundamental elements: embryo quality, endometrial receptivity in WOI and embryo-endometrial interaction [11-13]. Figure.2 but timing endometrial receptivity is still a challenge. These processes are controlled by different factors, including ovarian steroids and its receptors, cytokines, growth factors, adhesion molecules, transcriptional factors and many others [14]. The detection of WOI in every patient, in a personalized way, would be essential and would allow to increase pregnancy rates in ART. Failure of the endometrium to achieve receptivity and the timing of the receptive period are now recognised as important issues in the success of IVF [4].