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巨细胞外陷通过诱导肠道上皮细胞亡,在小鼠的DSS诱导的大肠炎中损害了肠道屏障功能

Ziqi Zhou¹, Xinyu Miao¹, Yiming Shen¹

¹School of Life Science and Technology, China Pharmaceutical University, Nanjing, China.

Biochemical pharmacology

|October 7, 2025

概括

巨细胞外陷 (METs),由PAD4驱动,通过增加结肠细胞死亡和屏障损伤,恶化性结肠炎 (UC). 抑制PAD4可以降低UC的严重程度,这表明METs是这种炎症性肠病的治疗点.

科学领域:

免疫学免疫学免疫学
胃肠病学胃肠病学
细胞生物学细胞生物学

背景情况:

性结肠炎 (UC) 是一种慢性炎症性肠病,其特征是结肠炎症.
巨细胞是UC病变发生的关键效应细胞.
巨细胞外陷 (METs),由基氨酸脱胺酶4 (PAD4) 介导,与炎症性疾病有关,但它们在UC中的作用尚不清楚.

研究的目的:

研究PAD4介导的MET形成在性结肠炎中的作用和机制.
确定MET是否有助于结肠上皮细胞亡和UC中的屏障功能障碍.
评估PAD4抑制作为UC的潜在治疗策略.

主要方法:

对UC患者的结肠组织中MET存在的分析以及DSS诱导的UC小鼠模型.
在结肠上皮细胞中评估亡.
通过RNA测序和西部斑分析,研究METs对MC38细胞中cGAS-STING通路和紧结蛋白的影响.
在PAD4淘汰赛小鼠中评估DSS诱导的大肠炎的严重程度.

主要成果:

在UC患者的结肠中,MET显著存在,并且与小鼠的结肠上皮细胞亡增加相关.
METs激活了MC38细胞中的cGAS-STING通路,导致细胞活力降低,细胞亡增强,并降低了紧结蛋白表达.
基因淘汰PAD4减弱了DSS诱导的大肠炎,减少了亡并改善了屏障功能.

结论:

PAD4介导的MET形成在性结肠炎的进展中起着重要作用.
METs通过诱导结肠上皮细胞亡和损害屏障功能来促进UC病变.
向PAD4和MET形成为性结肠炎治疗提供了一个有前途的治疗途径.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.肠道上皮细胞是肠道上皮细胞.巨细胞的细胞外陷乙氨基氨酸减小酶4 性结肠炎是一种 cGAS-STING 的使用情况.

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