BMP7 coordinates endometrial epithelial cell receptivity for blastocyst implantation through the endoglin pathway in cell lines and a mouse model.

Bone morphogenetic protein (BMP) expression has been observed in the uterus in previous studies. However, the influence of BMP7 on blastocyst implantation remains unclear. Blastocysts first act on luminal endometrial epithelial cells during implantation. The purpose of the present study was to explore the influence of BMP7 on endometrial epithelial cells. A pregnancy animal model, and mouse and human endometrial epithelial cells were used in the present study. Transient knockdown, immunofluorescence assay, embryo implantation, BMP7 silencing, reverse transcription-quantitative polymerase chain reaction, western blotting, immunoprecipitation and Rac1 function assay were also performed. It was revealed that BMP7 concentration was increased in endometrial epithelial cells during the final pre-receptive and receptive stages of receptivity in the mouse endometrium. Additionally, BM7 acted on the transforming growth factor-β receptor, endoglin. Endoglin expression was detected in both stromal and endothelial cells apart from trophoblast expression. Following knockdown of BMP7, Rac-GTP was decreased in endometrial epithelial cells and the uterus. Knockdown of endoglin by small interfering RNA decreased the number of blastocysts and implantation regions. Additionally, BMP7 silencing and endoglin suppression of Ishikawa cells led to impaired JAr spheroid attachment. These findings suggest that BMP7 is associated with receptivity of the endometrium, indicating that BMP7 regulates receptivity of endometrial epithelial cells for implantation of blastocysts via the endoglin pathway.