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Human Endometrial Mucin MUC1 Is Up-Regulated by Progesterone and Down-Regulated In Vitro by the Human Blastocyst
Ist Teil von
Biology of reproduction, 2001-02, Vol.64 (2), p.590-601
Ort / Verlag
Madison, WI: Society for the Study of Reproduction
Erscheinungsjahr
2001
Quelle
MEDLINE
Beschreibungen/Notizen
Expression of MUC1 in endometrial epithelium has been suggested to create a barrier to embryo attachment that must be lifted
at the time of implantation. In this study, we investigated the hormonal regulation of human endometrial MUC1 in hormone replacement
therapy cycles and in the human blastocyst. We also analyzed the embryonic regulation of MUC1 in human endometrial epithelial
cells (EECs) during the apposition and adhesion phases of human implantation using two different in vitro models. Our results
indicate that endometrial MUC1 mRNA and immunoreactive protein increase in receptive endometrium compared to nonreceptive
endometrium. Human blastocysts express MUC1, as demonstrated by reverse transcription-polymerase chain reaction and immunocytochemistry,
localized at the trophectoderm. In vitro, MUC1 was present at the surface of primary cultures of human EEC, and presence of
a human blastocyst (i.e., apposition phase) increases EEC MUC1 protein and mRNA compared to control EEC lacking embryos. Interestingly,
when human blastocysts were allowed to attach to the EEC monolayer (i.e., adhesion phase), MUC1 was locally removed in a paracrine
fashion on EEC at the implantation site. These results demonstrate a coordinated hormonal and embryonic regulation of EEC
MUC1. Progesterone combined with estradiol priming induces an up-regulation of MUC1 at the receptive endometrium. During the
apposition phase, presence of a human embryo increases EEC MUC1. However, at the adhesion phase, the embryo induces a paracrine
cleavage of EEC MUC1 at the implantation site. These findings strongly suggest that MUC1 may act as an endometrial antiadhesive
molecule that must be locally removed by the human blastocyst during the adhesion phase.