Uterine sensing of the embryo

Carson, Daniel D.

doi:10.1073/pnas.0503417102

Cited by 2 publications

(1 citation statement)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, targeted gene deletion of Wnt7a in mice results in the complete absence of uterine glands and infertility [28], and Fzd4-/-mice fail to become pregnant and exhibit impaired corpora lutea formation and function [12]. Under normal conditions, formation of the primary and secondary decidual zones may be driven by Wnt pathway activity [29]. Dkk2 normally functions as an antagonist of canonical Wnt signaling by binding to Kremen2 (Krm2) to inhibit betacatenin activity, but other data shows that Dkk2 can activate rather than inhibit the Wnt/β-catenin signaling pathway in Xenopus embryos [30].…”

Section: Discussionmentioning

confidence: 99%

Expression and Regulation of Dickkopf2 During Periimplantation in Mice

Zhang

Peng

Kuang

et al. 2009

Journal of Reproduction and Development

View full text Add to dashboard Cite

Abstract. Successful implantation depends on active dialogue between the maternal endometrium and the implanting blastocysts that is well controlled by groups of regulators at the molecular level. Dickkopf2 (Dkk2) is a member of Dickkopf family normally acting as an antagonist of canonical Wnt/beta-catenin signaling, which has been proven to participate in tumorigenesis and early embryo development. In order to explore the potential function of Dkk2 in embryo implantation, the present study investigated the uterine expression and regulation profiles of Dkk2 during periimplantation in mice. Using reverse transcription-polymerase chain reaction, immunohistochemistry and Western blotting, we showed that the mRNA and protein levels of Dkk2 began to increase in the glandular epithelium on day 4, continued to increase on day 5 and then decreased from day 6 of pregnancy. Moreover, on days 5-8 of pregnancy, Dkk2 was increasingly expressed in the deciduum of the uterus, especially around the implanting embryos. In addition, upregulation of Dkk2 was also observed in uteri treated with estrogen (estradiol-17β) as well as in oil-induced artificial decidualization, indicating that the expression of Dkk2 could be induced by both steroid hormone (estrogen) and the process of decidualization. Furthermore, in the postimplantation uterus, the Dkk2 protein showed an inversed expression with active beta-catenin from day 6 onward, supporting the notion that Dkk2 plays an inhibitory role against canonical Wnt signaling in the context of the decidualizing stroma. Collectively, our data suggests that Dkk2 expression is associated with uterine receptivity changes as well as the process of decidualization and that it might play important roles through inhibition of canonical Wnt signaling in the periimplantation uterus.

show abstract