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.

中文翻译：

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角质素86在植入过程中在子宫中被雌二醇诱导上调。

背景技术子宫的接受性是胚胎植入的决定因素之一，其决定妊娠成功的原因。通常在卵巢过度刺激引起的高雌激素患者中发现由于子宫接受力异常而导致的异常胚胎植入。结果本研究确定了角蛋白86（KRT86），一种纤维结构蛋白，在围植入期子宫内膜中被上调。使用先前研究中建立的高雌激素小鼠模型，我们发现植入前的异常雌二醇（E2）水平可能触发子宫上皮中Krt86的高表达。在卵巢切除的小鼠模型中，结合雌激素受体ERα和ERβ敲除小鼠模型，发现子宫Krt86在E2处理后由核ERα介导上调。此外，我们发现黄体酮（P4）可以改善由异常E2诱导的Krt86表达。结论这些结果揭示了Krt86的动态表达和调控，尤其是在雌激素治疗的小鼠中，表明其可能充当非接受性子宫的标志物。