Objective: To determine the effects of controlled ovarian hyperstimulation and resultant high levels of E(2) on endometrial HOXA10 expression (a marker of endometrial receptivity).
Design: Prospective study.
Setting: University academic medical center.
Patient(s): Twenty-five women undergoing controlled ovarian hyperstimulation with recombinant FSH and 30 fertile controls.
Intervention(s): Endometrium was obtained by Pipelle endometrial biopsy on cycle days 21-25. In addition, Ishikawa cells (a well-differentiated endometrial adenocarcinoma cell line) were treated with either E(2), recombinant FSH, GnRH agonist, or GnRH antagonist. RNA was extracted and analyzed by quantitative reverse transcriptase-polymerase chain reaction (RT-PCR).
Main outcome measure(s): HOXA10 expression.
Result(s): Endometrial HOXA10 expression in women undergoing controlled ovarian hyperstimulation (COH) with recombinant FSH was not different from that in fertile controls. Estradiol increased HOXA10 expression in Ishikawa cells in a dose-dependent manner from 10(-9) to 10(-7) M. Neither recombinant FSH, GnRH agonist, nor GnRH antagonist altered HOXA10 expression in these cells.
Conclusion(s): Controlled ovarian hyperstimulation did not inhibit endometrial HOXA10 expression in vivo. In addition, in vitro endometrial cell HOXA10 expression was not altered by either recombinant FSH, GnRH agonist, or GnRH antagonist. COH is unlikely to adversely impact endometrial receptivity.