角蛋白 86 在着床期间被雌激素诱导而在子宫中上调。

Keratin 86 is up-regulated in the uterus during implantation, induced by oestradiol.

机构信息

College of Basic Medical Sciences, Dalian Medical University, No. 9 West Section Lvshun South Road, Dalian, 116044, Liaoning, China.

Center for Reproduction and Health Development, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.

出版信息

BMC Dev Biol. 2020 Feb 7;20(1):3. doi: 10.1186/s12861-020-0208-6.

BACKGROUND

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.

RESULTS

This 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.

CONCLUSIONS

These 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.

背景

子宫容受性是胚胎着床的决定因素之一，它是妊娠成功的关键。由于子宫容受性紊乱导致的胚胎着床异常，通常发生在卵巢过度刺激引起的高雌激素患者中。

结果

本研究鉴定了角蛋白 86（KRT86），一种纤维结构蛋白，在着床期子宫子宫内膜中上调。使用之前研究中建立的高雌激素小鼠模型，我们发现异常的雌二醇（E2）水平在着床前可能会引发子宫上皮中 Krt86 的高表达。在去卵巢小鼠模型中，结合雌激素受体 ERα 和 ERβ 敲除小鼠模型，发现 E2 处理后子宫 Krt86 上调，由核 ERα 介导。此外，我们发现孕激素（P4）可改善异常 E2 诱导的 Krt86 表达。