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卵泡刺激激素通过上调ALKBH5表达来促进内皮细胞中的EndMT

Ping Li^1,2, Yixiao Xiang², Jinzhi Wei²

¹The Affiliated Qingyuan Hospital (Qingyuan People's Hospital), Guangzhou Medical University, Qingyuan, 511518, Guangdong, People's Republic of China.

Cellular & molecular biology letters

|April 4, 2025

概括

增加的卵泡刺激激素 (FSH) 通过诱导内皮细胞转化为介质细胞转化 (EndMT) 加快动脉样硬化. 这通过FSH上调ALKBH5发生,ALKBH5去甲基化FOXM1,促进EndMT和斑块不稳定.

科学领域:

心血管生物学心血管生物学
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

动脉样硬化发病率在绝经后增加,高囊刺激激素 (FSH) 加快了其进展.
内皮转介质转换 (EndMT) 加剧了斑块的不稳定性,这是急性冠状动脉综合征的关键因素.
FSH和EndMT之间的特定联系在很大程度上仍然没有被描述.

研究的目的:

调查FSH对EndMT的影响.
阐明FSH在动脉样硬化中可能调节EndMT的分子机制.

主要方法:

作为动脉样硬化模型,利用了阿波利波蛋白E缺陷 (ApoE-/-) 的小鼠和人类带血管内皮细胞 (HUVECs) 作为细胞模型.
使用免疫化学技术和RT-qPCR评估蛋白质和mRNA水平.
通过MeRIP和使用免疫沉的核酸-蛋白相互作用评估了m6A修饰状态.

主要成果:

发现毛囊刺激激素 (FSH) 在体外和体内都能诱导EndMT.
通过增强AlkB同位素5,RNA脱甲基酶 (ALKBH5) 的表达,FSH提高了叉头盒蛋白M1 (FOXM1) 的调节.
通过ALKBH5,FSH减少了FOXM1上的m6A修饰,增加了FOXM1的转录水平和稳定性,这是CREB促进的过程.

结论:

FSH促进ALKBH5的表达,导致FOXM1的N6-甲基氨酸 (m6A) 脱甲基化,并随后诱导EndMT.
这种机制突显了FSH在促进斑块不稳定的作用.
这些发现为预防绝经后妇女急性冠状动脉综合征提供了潜在的治疗点.

关键词:

在 ALKBH5H5 中内皮细胞向介质细胞的转变 (EndMT)在FOXM1中,卵泡刺激激素 (FSH) 是一种激素.

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