Abstract
BackgroundUterine receptivity is one of the determinants of embryo implantation, which is responsible for pregnancy success. Aberrant embryo implantation due to disrupted uterine receptivity is usually found in ovarian hyperstimulation induced hyperoestrogen patients.ResultsThis study identified keratin 86 (KRT86), a fibrous structural protein, which was upregulated in uterine endometrium during peri-implantation. Using a hyperoestrogen mouse model established in a previous study, we found abnormal oestradiol (E2) levels during pre-implantation could trigger high expression of Krt86 in the uterine epithelium. In an ovariectomised mouse model, combining oestrogen receptors ERα and ERβ knockout mice models, uterine Krt86 was found to be up-regulated after E2 treatment, mediated by nuclear ERα. Furthermore, we found progesterone (P4) could ameliorate Krt86 expression, induced by abnormal E2.ConclusionsThese results revealed the dynamic expression and regulation of Krt86, especially in hyperoestrogen treated mice, indicating it might act as a marker for non-receptive uterus.
Highlights
Uterine receptivity is one of the determinants of embryo implantation, which is responsible for pregnancy success
In the current study, using hyperoestrogen and ovariectomised mouse models, we found that Krt86 was expressed during embryo implantation, and was up-regulated by E2 through the nuclear oestrogen receptor ERα pathway
keratin 86 (KRT86) was localised to the epithelium of uteri (Fig. 2c, d), compared with the oestrogen receptor antagonist ICI 182780 treated group (Fig. 2e, f), suggesting that KRT86 might play a role in hyperoestrogen-induced uteri
Summary
Uterine receptivity is one of the determinants of embryo implantation, which is responsible for pregnancy success. Aberrant embryo implantation due to disrupted uterine receptivity is usually found in ovarian hyperstimulation induced hyperoestrogen patients. Embryo implantation establishes pregnancy [1]. Regulated progesterone (P4) and oestrogen (E2) determine uterine receptivity and embryo implantation. In mice, increased ovarian P4 insures uterine receptivity, and a small surge of oestrogen triggers the initiation of embryo implantation. Disturbances of P4 and E2 during this process can affect implantation, for example, hyperoestrogen induced by ovarian hyperstimulation in in vitro fertilisation (IVF) treatment disrupts embryo implantation. Different genes have been found to participate in uterine receptivity and embryo implantation regulation, gene changes under the stress of implantation remain less well-known. Given that implantation could be considered a form of xenoimplantation, proteins which regulate epithelial cell sensing and that protect against outside stress may participate in
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