Mu Hui, Yu Haikun, Yan Song, Lu Jie, Mao Jiaqin, Sun Dan, Jin Ni, Fang Zheng, Lu Xueyan, Dong Jie, Su Ying, Chen Shuqiang, Wang Xiaohong
Reproductive Medicine Center, Department of Gynecology and Obstetrics, Tangdu Hospital, Air Force Medical University, No.1 Xinsi Road, Baqiao District, Xi'an, Shaanxi, China.
Clinical Research Center for Reproductive Medicine and Gynecological Endocrine Diseases of Shaanxi Province, Xi'an, Shaanxi, China.
J Assist Reprod Genet. 2024 Nov;41(11):3189-3200. doi: 10.1007/s10815-024-03241-3. Epub 2024 Sep 14.
High serum estrogen concentrations after controlled ovarian hyperstimulation (COH) and fresh embryo transfers are associated with the increased risk of pregnancy complications resulting from aberrant placentation. Uterine natural killer (uNK) cells are important for establishment of pregnancy and normal placentation. It has been found that the proliferation and function of uNK cells are compromised by COH. However, the underlying role of high concentration of estrogen following COH in the abnormalities of uNK cells is poorly understood.
Expression of cytokines and immunophenotype study of uNK was performed by flow cytometry analysis. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to quantify RNA expression; Western blot was performed to quantify protein levels.
The secretion level of pro-angiogenic factors in uNK cells is significantly reduced by co-culture with decidual stromal cells (DSCs) induced by high estrogen. It was discovered that COH and supraphysiologic levels of estrogen downregulated IL-11 in decidual tissue of mice. Additionally, we found that the downregulation of IL-11 is a major factor contributing to the downregulation of VEGF and PLGF in uNK cells. Moreover, we found that uNK cells may acquire IL-11Rα sequentially during differentiation and that only a portion of uNK cells are IL-11Rα positive. Lastly, we discovered that IL-11 may regulate VEGF and PLGF secretion in uNK cells via the ERK signaling pathway.
These results suggested the downregulation of IL-11 expression in DSCs caused by high estrogen levels affects the secretion of pro-angiogenic factors in uNK cells, which provided an explanation for the pregnancy complications caused by COH.
控制性卵巢刺激(COH)及新鲜胚胎移植后血清雌激素浓度升高与胎盘植入异常导致的妊娠并发症风险增加相关。子宫自然杀伤(uNK)细胞对妊娠的建立及正常胎盘植入至关重要。已发现COH会损害uNK细胞的增殖和功能。然而,COH后高浓度雌激素在uNK细胞异常中的潜在作用尚不清楚。
通过流式细胞术分析进行细胞因子表达及uNK免疫表型研究。采用定量实时聚合酶链反应(qRT-PCR)定量RNA表达;采用蛋白质免疫印迹法定量蛋白质水平。
与高雌激素诱导的蜕膜间质细胞(DSCs)共培养可显著降低uNK细胞中促血管生成因子的分泌水平。研究发现,COH及超生理水平的雌激素可下调小鼠蜕膜组织中的IL-11。此外,我们发现IL-11的下调是导致uNK细胞中VEGF和PLGF下调的主要因素。而且,我们发现uNK细胞在分化过程中可能依次获得IL-11Rα,且只有一部分uNK细胞是IL-11Rα阳性。最后,我们发现IL-11可能通过ERK信号通路调节uNK细胞中VEGF和PLGF的分泌。
这些结果表明,高雌激素水平导致DSCs中IL-11表达下调,影响了uNK细胞中促血管生成因子的分泌,这为COH导致的妊娠并发症提供了解释。