Abstract
Uterine receptivity is defined as a state when the uterine milieu is favorable for blastocyst implantation and it can only last for a limited time period. In this study, by utilizing the embryo transfer model, it was observed that a portion of blastocysts could initiate implantation even when transferred beyond the timing of normal uterine receptivity, while their mid-gestational embryo development exhibited severe retardation, suggesting that the uterine status beyond the normal implantation window is unconducive for normal implantation. We further performed microarray analysis to explore the molecular basis that distinguishes the normal and defective uterine receptivity. A total of 229 genes was found to be differentially expressed, and a large amount of them were epithelium-expressing genes and responsive to progesterone signaling.
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