Maternal-foetal communication is essential during implantation for ensuring coordinated changes in luminal uterine epithelial cells (UECs) and trophoblastic cells of the blastocyst. The morphological appearance of vesicles in the apical cytoplasm of receptive UECs, and the uptake of tracer into the uterine epithelium at the time of uterine receptivity indicates endocytosis is occurring in these cells. Endocytosis can occur through clathrin-dependant or clathrin-independent means. Caveolin-1, a protein involved in clathrin-independent endocytosis, and morphological caveoli are found on the basolateral membrane of rat UECs at the time of uterine receptivity suggesting a role for clathrin-independent endocytosis. There is however less information on clathrin-dependant endocytosis in uterine epithelial cells during uterine receptivity.

Intersectin-2 (ITSN2) and Endophilin A2 (EA2) are proteins involved in clathrin-mediated endocytosis. This study investigated the localisation of ITSN2 and EA2 in uterine epithelial cells in vivo and in vitro. Both ITSN2 and EA2 were found to increase in UECs at the time of receptivity in the rat. When endocytosis was inhibited by Dynasore (a dynamin inhibitor) there was a decrease in fluorescent staining of EA2 in receptive RL-95 cells in vitro.  In an in vitro co-culture system of receptive Ishikawa cells and JEG-3 spheroids, we observed a decrease in spheroid adherence after treatment with Dynasore. These studies suggest an important role of clathrin-mediated endocytosis in uterine epithelial cells during blastocyst attachment. A deeper understanding of the mechanisms that regulate communication at the maternal-foetal interface may provide novel mechanisms for improving pregnancy rates.