Endoglin (CD105) coordinates the process of endometrial receptivity for embryo implantation

• Endoglin expressed predominantly in the implantation sites in the uterus.
• Endoglin was seen associated with primary and secondary decidual zone.
• Delayed receptivity of endometrium reduced the endoglin in epithelial as well as stromal cells.
• Transient knockdown of endoglin of endometrial tissue can render blockage of embryo implantation.
• Depletion of endoglin from endometrial epithelial cells negatively affected blastocyst attachment reaction.

Endoglin is a TGF-β receptor that is expressed in uterine endothelial and stromal cells in addition to trophoblast expression. However, the functional importance of endoglin in the embryo implantation process is not clear. We observed endoglin expression in the endometrium throughout the stages of its receptivity; however, its expression was enhanced during the receptive stage. Endoglin expression was predominant in epithelial cells of the lumen and glands, but showed a milder expression in stromal cells. Endoglin expression was initially observed in the primary decidual zone and later extended to the secondary decidua zone. Knockdown of endoglin via siRNA reduced the implantation sites along with the blastocyst numbers. Mouse blastocyst with endoglin-silenced endometrial epithelial cells (human and mouse origin) showed poor trophoblast outgrowth, which suggests an essential role for endoglin during endometrial receptivity. In conclusion, our findings reveal the association of endoglin with endometrial receptivity, which is important for embryo attachment.