Introduction

Recurrent implantation failure (RIF) is a challenging problem of assisted reproductive technology that arises mainly due to inadequate endometrial receptivity and its pathogenesis is still unclear.

Objectives

In this study, we conducted the first investigation of the effect of decreased PIBF1 expression in mid-secretory phase on endometrial receptivity in patients with RIF.

Methods

Microarray assay, reverse transcriptase-quantitative polymerase chain reaction, western blot, and in-vitro experiments were conducted.

Results

The results showed that progesterone-induced blocking factor 1 (PIBF1) expression was highest in the mid-secretory endometrium in control subjects, but was significantly lower in RIF patients. In Ishikawa and human endometrial stromal cells (HESCs), rather than human endometrial epithelial cells, PIBF1 knockdown significantly downregulated cell proliferation and the levels of interleukin 6 (IL6) and phosphorylated signal transducer and activator of transcription-3 (p-STAT3). Besides, in HESCs, the levels of IL6, p-STAT3, prolactin and insulin-like growth factor binding-protein-1 (IGFBP1) decreased after PIBF1 knockdown during in-vitro decidualization. All these cellular changes could be notably restored by PIBF1 or IL6 overexpression. Consistent with our findings with PIBF1, the levels of IL6, p-STAT3, ki-67, prolactin, and IGFBP1 in the mid-secretory endometrium were notably lower in patients with RIF compared with controls.

Conclusion

In summary, in the mid-secretory phase, decreased expression of PIBF1, IL6, and p-STAT3 inhibited HESC proliferation and decidualization, which is of theoretical and clinical importance for future research and clinical-treatment strategies.

中文翻译：

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分泌中期PIBF1/IL6/p-STAT3减少抑制人子宫内膜基质细胞增殖和蜕膜化

介绍

复发性着床失败（RIF）是辅助生殖技术中的一个具有挑战性的问题，主要是由于子宫内膜容受性不足而引起的，其发病机制尚不清楚。

目标

在这项研究中，我们首次调查了分泌中期 PIBF1 表达降低对 RIF 患者子宫内膜容受性的影响。

方法

进行了微阵列分析、逆转录酶定量聚合酶链反应、蛋白质印迹和体外实验。

结果

结果显示，孕酮诱导的阻滞因子 1 (PIBF1) 表达在对照组的中分泌子宫内膜中最高，但在 RIF 患者中显着较低。在 Ishikawa 和人类子宫内膜基质细胞 (HESC) 中，PIBF1 敲低显着下调细胞增殖和白细胞介素 6 (IL6) 和磷酸化信号转导和转录激活因子 3 (p-STAT3) 的水平，而不是人类子宫内膜上皮细胞。此外，在 HESCs 中，在体外蜕膜过程中敲低 PIBF1 后，IL6、p-STAT3、催乳素和胰岛素样生长因子结合蛋白-1（IGFBP1）的水平降低。所有这些细胞变化都可以通过 PIBF1 或 IL6 过表达显着恢复。与我们对 PIBF1 的发现一致，IL6、p-STAT3、ki-67、催乳素、

结论

总之，在分泌中期，PIBF1、IL6和p-STAT3的表达降低抑制了HESC的增殖和蜕膜化，这对未来的研究和临床治疗策略具有理论和临床意义。