Impact of endometrial claudin-3 deletion on murine implantation, decidualization, and embryo development†

Though claudin-3-deficient mice are fertile, endometrial deletion of claudin-3 impairs decidualization leading to reduced size of implantation sites in early pregnancy and to a decrease in prenatal fetal weight. The composition of cell contacts in the endometrium plays an important role in the process of embryo implantation and the establishment of pregnancy. In previous studies, we showed an induction of the tight junction protein claudin-3 in the developing decidua from day 6.5 of pregnancy onward. To evaluate the role of this specific claudin-3 distribution, we here evaluated the effect of an endometrial claudin-3 deletion in implantation and embryo development in claudin-3 knockout mice. Claudin-3 knockout mice were fertile but revealed a slightly reduced amount of implantation sites as well as of litter size. Though implantation sites showed morphologically regularly developed embryos and deciduas, depth of ectoplacental cone invasion was reduced in tendency compared to controls. The weight of the implantation sites on day 6.5 and 8.5 of pregnancy as well as the weight of the embryos on day 17.5 of pregnancy, but not of the placentas, was significantly reduced in claudin-3 knockout mice due to a maternal effect. This could be due to an impairment of decidualization as substantiated by a downregulation of the transcription of various decidua-associated genes in the early implantation sites of claudin-3 knockout mice. The fact that claudin-3 knockout mice are nevertheless fertile possibly may be compensated by the presence of other claudins like claudin-4 and claudin-10.

Automated summary

Deletion of claudin-3 in the endometrium impairs decidualization and leads to reduced size of implantation sites and fetal weight. Transcription downregulation of various decidua-associated genes may contribute to the impairment of decidualization.