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孕激素在树叶层细胞中的不活化:炎症诱导分娩的机制

Angela DeTomaso^1,2, Hyeyon Kim², Jacqueline Shauh²

¹Department of Pathology, Case Western Reserve University, Cleveland, OH 44106.

Proceedings of the National Academy of Sciences of the United States of America

|June 11, 2024

概括

胎儿 - 母亲界面的炎症通过通过AKR1C1在叶 stromal 细胞中通过激活孕激素 (P4) 来诱导分娩. 抑制AKR1C1可能会防止早产.

科学领域:

生殖生物学生殖生物学
免疫学免疫学免疫学
生物化学生物化学

背景情况:

人类分娩涉及胆管-决定性接口 (CDI) 的炎症.
孕激素 (P4) 通常会抑制分娩,但炎症可能会抵消这种效应.
断层层细胞 (DS) 和免疫细胞是CDI的关键参与者.

研究的目的:

为了测试CDI的炎症是否通过否定P4的抑制能力来诱导分娩.
为了研究阿尔多基因还原酶家族1成员C1 (AKR1C1) 在P4无活化中的作用.
探索AKR1C1抑制作为早产的治疗策略.

主要方法:

在分娩期间分析了人类, rhesus macaque 和老鼠 CDI 中的 AKR1C1 表达.
使用了人类DS细胞系和术语人类胎儿膜扩展剂.
研究了互白素-1ß (IL-1ß),LPS刺激的巨细胞和AKR1C1抑制对P4水平和反应能力的影响.

主要成果:

在不同物种中,AKR1C1的表达随着长期和早产而增加.
IL-1β和巨受条件介质增加了AKR1C1的表达,并降低了DS细胞中的P4水平/响应能力.
在小鼠中,AKR1C1的抑制或绕过恢复了P4的反应能力,并防止了炎症诱导的早产.

结论:

在CDI的炎症通过诱导DS细胞中的AKR1C1-介导的P4无活化来驱动分娩.
P4 的AKR1C1 失活是分娩中的关键机制.
抑制或绕过AKR1C1为与炎症相关的早产提供了潜在的治疗方法.

关键词:

这是一种炎症炎症炎症炎症.产妇分娩产妇分娩怀孕怀孕怀孕怀孕怀孕孕激素代谢的代谢过程

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