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C/EBPδ 缺陷延迟了感染引起的早产

Wen-Jia Lei^1,2, Fan Zhang^1,2, Meng-Die Li^1,2

¹Center for Reproductive Medicine, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.

|October 8, 2024

概括

CCAAT增强剂结合蛋白 δ (C/EBPδ) 在感染诱导的早产中维持炎症. 准C/EBPδ提供了一种潜在的治疗策略,可以预防早产,特别是当感染开始时.

科学领域:

生殖生物学生殖生物学
免疫学免疫学免疫学
遗传学是一个遗传学.

背景情况:

分娩涉及炎症过程,在感染期间的过度反应可能导致早产.
核因子kappa B (NF-κB) 是已知的炎症反应的调解者,但其作用通常是短暂的.
其他转录因子可能参与在感染诱导的早产期间维持NF-κB发起的妊娠组织炎症.

研究的目的:

研究CCAAT增强剂结合蛋白 δ (C/EBPδ) 在脂聚糖 (LPS) 诱导的早产中的作用.
剖析胎儿和母亲C/EBPδ对早产的不同贡献.
探索C/EBPδ对人类和小鼠肌胎和羊膜细胞分娩相关过程的影响.

主要方法:

生产CCAAT增强剂结合蛋白δ (C/EBPδ) 缺乏的小鼠,以研究其在脂聚糖 (LPS) 诱导的早产中的作用.
使用野生类型 (WT) 和C/EBPδ缺乏的胚胎和母体进行交叉培养实验,以确定胎儿和母亲的贡献.
分析C/EBPδ表达和功能在小鼠和人类肌肉细胞和羊膜细胞,并检查其与人类羊膜纤维细胞中NF-κB的相互作用.

主要成果:

胚胎或母体中C/EBPδ的缺陷,在小鼠中延迟了LPS诱导的早产,当两者都缺乏时,延迟更为明显.
在小鼠和人类样本中,在感染引起的早产期间,在子宫膜和胎儿膜中观察到C/EBPδ的丰度增加.
C/EBPδ促进了LPS诱导的促炎细胞因子和与肌体收缩性和胎儿膜激活相关的基因的上调. 在机理上,C/EBPδ作为NF-κB的补充转录因子,维持与分娩相关基因的表达.

结论:

在感染诱导的早产期间,CCAAT增强剂结合蛋白 δ (C/EBPδ) 作为一个转录因子,在子宫和胎儿膜中维持NF-κB启动的基因表达.
准C/EBPδ为管理和治疗感染引起的早产提供了潜在的治疗途径.

关键词:

C/EBPδ 在线阅读胎儿的膜胎儿的膜炎症炎症是一种炎症.这种表达方式是Myometrium.这就是NF-κBB.分割的方法分割的方法过早分娩过早分娩是什么

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