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在肺损伤修复过程中,AP-1介导的染色质变化控制着膜2型细胞的转变

Anne M Lynch, Tala Noun, Sujuan Yang

bioRxiv : the preprint server for biology

|November 24, 2025

概括

肺干细胞 (AT2) 在受伤时激活,过渡到再生状态. 激活蛋白-1 (AP-1) 转录因子驱动这种AT2细胞过渡,影响修复,并可能导致肺癌的发展.

科学领域:

细胞生物学细胞生物学
干细胞生物学干细胞生物学
分子生物学分子生物学

背景情况:

选择性干细胞,就像肺膜类型2 (AT2) 细胞一样,在专门和塑性状态之间切换以进行组织修复.
控制这种AT2细胞可塑性的分子机制及其在再生与病理结局中的作用仍然不完全理解.

研究的目的:

阐明调节肺损伤和修复期间AT2细胞过渡的分子开关和表观遗传变化.
研究激活蛋白-1 (AP-1) 转录因子在调解AT2细胞可塑性和分化中的作用.

主要方法:

在小鼠模型中进行多组基因分析 (转录基因和表观基因).
鼠标遗传学评估AP-1成员 (FOS,FOSB,JUNB) 的功能.
免疫染和人类肺部组织的分析与前恶性或腺癌病变.

主要成果:

AP-1转录因子 (FOS,FOSB,JUNB) 促进受伤诱导的过渡性AT2细胞状态,具有独特的染色质景观.
鉴定出了一种CLDN4+AT2细胞子集,具有高KRT8表达和为AP-1基因丰富的开放色素.
AP-1激活对于AT2细胞分散,纤维细胞信号传递和区域特定的AT1分化是必需的,并且在瘤性Kras驱动的肺瘤发生和人类肺癌中被保留.

结论:

AP-1转录因子是AT2细胞命运过渡,桥梁组织修复和瘤发生的关键调节者.
这项研究完善了对AT2过渡细胞状态及其相关表观遗传动态的理解.
保存的分子逻辑将肺修复机制与瘤转化联系在一起,突出显示了AP-1的核心作用.

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