The embryonic development of all eutherian mammals occurs in the uterus, where they acquire continuous nutrition support from their mothers. The physical connection between the embryos and the mother is first established during implantation, where the blastocysts attach and invade into the uterine wall as a result of comprehensive molecular communication between the two parts. In order for this to occur, the uterus must be properly prepared to become transiently receptive to the approaching blastocysts. This so called window of receptivity or uterine receptivity, is preceded by a pre-receptive phase when the uterus is yet ready to allow implantation, and is followed by a refractory phase. The receptivity of the uterus is subject to the regulation by genetic and environmental factors, and is a major etiology for human infertility. Although substantial effort has been invested, more work is required to understand the molecular pathways involved in establishing uterine receptivity. The success of embryo implantation depends on the receptivity of the uterus. Abdominal B class homeobox gene Hoxa10 is dynamically expressed around implantation, and is indispensable for establishing uterine receptivity. However, the exact mechanism through which HOXA10 exerts its function remains elusive. In this report, we investigated the molecular basis for the implantation failure caused by Hoxa10 deficiency using both knock-out mouse models and global gene expression profiling approaches. We demonstrated that augmented local immune response through T/B cells alone is not sufficient to explain the implantation defects observed in the Hoxa10-null uterus. We also uncovered a group of potential genes and signaling pathways that may participate in the downstream events mediated by HOXA10. Molecular Analysis of Implantation Defects in Homeobox Gene Hoxa10-Deficient Mice: Yan Yin, Congxing Lin, Dima Sawalha, Brent M. Bany and Liang Ma.
Last date updated on June, 2014