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雌激素诱导的YAP1激活在自发的早产中破坏了胆管 trofhoblast 屏障的完整性

Qimei Lin¹, Jiasong Cao¹, Yu Zhu²

¹Tianjin Institute of Gynaecology Obsterics, Tianjin Central Hospital of Gynaecology Obstetrics & Nankai University Affiliated Maternity Hospital, Tianjin, 300100, China; Tianjin Key Laboratory of Human Development and Reproductive Regulation, Tianjin Central Hospital of Gynaecology Obstetrics, Tianjin, 300100, China.

|July 11, 2025

概括

激素信号破坏胆管 trofhoblast 细胞屏障,导致自发早产 (sPTL). 在怀孕第二季度早期发现雌激醇 (E2) 和PAI-1的升高,可以预测sPTL风险.

科学领域:

生殖生物学和内分泌学.
产科和孕产妇和胎儿医学
劳动的细胞和分子机制.

背景情况:

胆管 trofhoblast 细胞 (CTC) 屏障稳态对于怀孕的维持至关重要.
荷尔蒙失衡和免疫功能障碍已知是导致早产的因素.
身体屏障功能障碍在带有完整膜 (sPTL) 的自发早产中所起的作用尚不清楚.

研究的目的:

调查sPTL中CTC屏障的物理完整性.
阐明17β-雌二醇 (E2) /YAP1信号在CTC屏障功能障碍中的作用.
为了确定早期sPTL预测的潜在生物标志物.

主要方法:

比较CTC屏障完整性生物标志物 (组织病理学,细胞结,TEER) 在非分娩期 (TNL),sPTL和分娩期 (TL) 组.
研究了激活的E2/YAP1信号对人类初级CTCs (phCTCs) 和胆管探索物的影响.
使用ELISA测量了血E2和PAI-1度.

主要成果:

sPTL和TL组显示CTC屏障破坏,减少TEER,减少细胞结蛋白.
增加的YAP1表达和核定位与增加的CTC迁移和透性相关.
E2通过ERα激活YAP1,促进屏障破坏;抑制减轻了损伤. 第二个三个月的E2和PAI-1预测了sPTL (AUC=0.894).

结论:

激活的E2/ERα-YAP1信号破坏了CTC的完整性,导致sPTL.
在第二个三个月的联合E2和PAI-1测量可以潜在地识别sPTL的高风险怀孕.
这一发现为早期的sPTL风险评估提供了新的途径.

关键词:

障碍物损坏障碍物损坏障碍物损坏胆管 trofhoblast 细胞细胞的细胞.在 KRT6AA 里.类似细胞的透性这是自发的早产.一个YAP1一个YAP1

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