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在腺菌症中异常的TCF21上调会通过增加PDE4C表达来损害子宫内膜分泌

Ruoer Yu¹, Chenxuan Wei¹, Guojing Li¹

¹International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200030, China; Shanghai Key Laboratory of Embryo Original Diseases, Shanghai 200030, China; Municipal Key Clinical Specialty, Shanghai 200030, China.

Biochimica et biophysica acta. Molecular basis of disease

|September 26, 2024

概括

转录因子21 (TCF21) 在腺菌症 (AM) 患者中升高,损害了决策. TCF21破坏了PDE4C/cAMP-FOXO1通路,为改善AM的生育提供了一个目标.

科学领域:

生殖生物学和内分泌学.
分子遗传学和细胞信号传递
不孕症的研究研究.

背景情况:

损伤的决定性是腺菌症 (AM) 中不孕症的主要原因.
转录因子21 (TCF21) 在AM中的作用及其对决定性的影响在很大程度上是未知的.
了解TCF21的机制对于改善AM患者的生殖结果至关重要.

研究的目的:

研究AM患者子宫内膜组织中的TCF21表达.
阐明TCF21损害人类子宫内膜层细胞 (HESC) 脱细胞化的机制.
确定潜在的治疗点,以增强与AM相关的不孕症中的子宫内膜受容性.

主要方法:

转录组分析以比较对照组和AM相关的复发性植入失败 (RIF) 组之间的基因表达.
定量实时PCR (qRT-PCR),西斑和免疫组织化学 (IHC) 来确认TCF21的表达和定位.
RNA测序 (RNA-seq),染色体免疫沉降测序 (ChIP-seq) /qPCR和双露西法酶记者分析以确定分子变化和TCF21-PDE4C相互作用.

主要成果:

与对照组相比,AM-RIF患者的子宫内膜中TCF21表达显著更高.
在HESC中过度表达TCF21,抑制了果标记物和改变了细胞骨架,损害了果化.
从机制上讲,TCF21通过上调PDE4C和下调FOXO1表达来抑制细胞内cAMP水平.

结论:

在AM患者中,TCF21通过PDE4C/cAMP-FOXO1信号轴损害了决定性.
这一途径为AM中与决定性化相关的不孕症的病理学提供了关键的见解.
准TCF21介导途径是一个潜在的治疗策略,可以改善子宫内膜受体.

关键词:

这是一个PDE4C.在TCF2121中,我们可以看到:腺菌症的发生.个人化的决定性.胚胎内膜的 stromal 细胞.

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