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Brd4通过调节高脂肪饮食养小鼠的结肠巨细胞透来调节代谢内毒素引起的炎症

Jinfeng Hu¹, Guo Li¹, Xiaoxin He¹

¹Fujian Key Laboratory of Translational Research in Cancer and Neurodegenerative Diseases, Institute for Basic Medical Sciences, School of Basic Medical Sciences, Fujian Medical University, Fuzhou, China.

Communications biology

|December 29, 2024

概括

表观遗传因子Brd4通过控制结肠巨细胞活动,驱动高脂肪饮食引起的炎症和肥胖. 抑制Brd4可能是对抗代谢障碍的策略.

科学领域:

分子生物学分子生物学
免疫学免疫学免疫学
代谢过程中的代谢.

背景情况:

高脂肪饮食 (HFD) 引发慢性炎症,肥胖和胰岛素抵抗.
人们还没有完全理解HFD诱导的代谢炎症背后的确切机制.

研究的目的:

研究表观遗传因子Brd4在HFD诱导的代谢炎症中的作用.
探索Brd4对结肠巨细胞活动的调节及其对代谢健康的影响.

主要方法:

在食HFD的小鼠中利用了骨髓系特异的Brd4删除 (Brd4-CKO).
分析了结肠炎症,巨细胞透和基因表达 (Ccr2/Ccr5).
研究了 Brd4 涉及 NF-κB 和增强 RNA 在巨细胞迁移中的机制.

主要成果:

在HFD下,Brd4-CKO小鼠表现出减少的结肠炎症和巨细胞透.
Brd4删除降低了Ccr2和Ccr5的表达,损害了巨细胞的迁移.
在Brd4-CKO小鼠中减少了巨细胞透,改善了肠道屏障功能,降低了代谢性内毒症.
在LPS挑战后,Brd4-CKO小鼠显示恢复了对HFD诱导的肥胖和胰岛素耐药性的敏感性.

结论:

在对HFD的反应中,Brd4是结肠巨细胞介导炎症和代谢性内毒症的关键发起者.
Brd4代表了HFD诱导的炎症,肥胖和相关的代谢并发症的潜在治疗标.

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