Abstract
BackgroundUnderstanding the molecular basis of embryonic implantation is of great clinical and biological relevance. Little is currently known about the adhesion receptors that determine endometrial receptivity for embryonic implantation in humans.Methods and Principal FindingsUsing two human endometrial cell lines characterized by low and high receptivity, we identified the membrane receptor CD98 as a novel molecule selectively and significantly associated with the receptive phenotype. In human endometrial samples, CD98 was the only molecule studied whose expression was restricted to the implantation window in human endometrial tissue. CD98 expression was restricted to the apical surface and included in tetraspanin-enriched microdomains of primary endometrial epithelial cells, as demonstrated by the biochemical association between CD98 and tetraspanin CD9. CD98 expression was induced in vitro by treatment of primary endometrial epithelial cells with human chorionic gonadotropin, 17-β-estradiol, LIF or EGF. Endometrial overexpression of CD98 or tetraspanin CD9 greatly enhanced mouse blastocyst adhesion, while their siRNA-mediated depletion reduced the blastocyst adhesion rate.ConclusionsThese results indicate that CD98, a component of tetraspanin-enriched microdomains, appears to be an important determinant of human endometrial receptivity during the implantation window.
Highlights
Endometrial receptivity is a self-limited period in which the endometrial epithelium acquires a functional and transient ovarian steroid-dependent status that allows blastocyst adhesion [1]
These results indicate that CD98, a component of tetraspanin-enriched microdomains, appears to be an important determinant of human endometrial receptivity during the implantation window
The genomics of human endometrial receptivity has been explored in natural cycles [6,7,8] but different genes have been proposed to be essential for receptivity, none has been found to have a clinical application, and evidence of function is in many cases lacking
Summary
Endometrial receptivity is a self-limited period in which the endometrial epithelium acquires a functional and transient ovarian steroid-dependent status that allows blastocyst adhesion [1]. This period, termed the ‘‘implantation window’’, lasts from 4–5 days to 9–10 days after progesterone production or administration. The genomics of human endometrial receptivity has been explored in natural cycles [6,7,8] but different genes have been proposed to be essential for receptivity (see [9] for review), none has been found to have a clinical application, and evidence of function is in many cases lacking. Little is currently known about the adhesion receptors that determine endometrial receptivity for embryonic implantation in humans
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