Abstract
The mouse is a widely used animal model for studying human reproduction. Although global gene expression changes associated with human uterine receptivity have been determined by independent groups, the same studies in the mouse are scarce. The extent of similarities/differences between mice and humans on uterine receptivity at the molecular level remains to be determined. In the present study, we analyzed global gene expression changes in receptive uterus on day 4 of pregnancy compared to non-receptive uterus on day 3 of pregnancy in mice. A total of 541 differentially expressed genes were identified, of which 316 genes were up-regulated and 225 genes were down-regulated in receptive uterus compared to non-receptive uterus. Gene ontology and gene network analysis highlighted the activation of inflammatory response in the receptive uterus. By analyzing the promoter sequences of differentially expressed genes, we identified 12 causal transcription factors. Through connectivity map (CMap) analysis, we revealed several compounds with potential anti-receptivity activity. Finally, we performed a cross-species comparison against human uterine receptivity from a published dataset. Our study provides a valuable resource for understanding the molecular mechanism underlying uterine receptivity in mice.
Highlights
Embryo implantation into the uterus is a crucial process for human pregnancy (Wang and Dey, 2006)
Our study provides a valuable resource for understanding the molecular mechanism underlying uterine receptivity in mice
In order to capture global gene expression changes associated with uterine receptivity in mice, RNA-seq data were generated from the pre-receptive/non-receptive uterus on day 3 and receptive uterus on day 4 of pregnancy, with three biological replicates, respectively
Summary
Embryo implantation into the uterus is a crucial process for human pregnancy (Wang and Dey, 2006). Human embryo implantation is a relatively low-efficiency process. It has been demonstrated that the maximum chance of pregnancy occurring in a menstrual cycle is approximately 30%, largely due to implantation failure (Wilcox et al, 1993; Zinaman et al, 1996). Successful implantation requires both an implantation competent blastocyst and a receptive endometrium. Embryo defect is responsible for two thirds of implantation failures, inadequate uterine receptivity has been estimated to contribute to the other one third (Macklon et al, 2006). It is imperative to understand the molecular mechanism underlying uterine receptivity
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