CTRP6促进巨细胞的炎症反应,其缺乏会减轻LPS诱导的炎症
Cheng Xu1, Dylan C Sarver1, Xia Lei2
1Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
The Journal of biological chemistry
|December 16, 2023
概括
蛋白CTRP6 (C1q/TNF相关蛋白6) 激活了巨细胞中的炎症基因程序和信号通路,促进了与肥胖相关的炎症. 失去CTRP6会抑制炎症反应,这表明它在调节组织炎症方面发挥了作用.
科学领域:
- 免疫学 免疫学 免疫学
- 代谢性疾病是一种代谢性疾病.
背景情况:
- 巨细胞是炎症和组织平衡的关键调节者.
- CTRP6 (C1q/TNF相关蛋白6号) 与肥胖相关的炎症有关.
- 目前尚不完全了解CTRP6影响巨细胞功能的精确机制.
研究的目的:
- 阐明巨细胞中由CTRP6调节的基因程序和信号通路.
- 研究CTRP6在巨细胞炎症反应和代谢转变中的作用.
主要方法:
- 对小鼠骨髓衍生的巨细胞 (BMDMs) 的转录和蛋白分析.
- 药理上抑制MAPK和NF-κB信号通路.
- 评估巨细胞对LPS刺激的反应.
- 来自CTRP6缺乏小鼠的BMDMs的分析.
- 用小鼠进行体内研究,以评估LPS诱导的炎症和低温.
主要成果:
- 在BMDM中,CTRP6治疗上调了促炎和抑制了抗炎基因表达.
- CTRP6激活了p44/42-MAPK,p38-MAPK和NF-κB信号,增强了细胞因子的分泌.
- CTRP6促进了有氧糖解,降低了氧化代谢,并增加了线粒体ROS的产生.
- 来自CTRP6缺乏的小鼠的BMDM显示出基线炎症减少和抑制LPS诱导的反应.
- 在小鼠中失去CTRP6减轻了LPS诱导的炎症和低温.
结论:
- CTRP6激活炎症通路,并启动巨细胞,以增加对炎症刺激的反应.
- CTRP6影响巨细胞的新陈代谢,使其转向一种促炎性表型.
- 在体外和体内,CTRP6在调节巨细胞介导炎症方面发挥着重要作用.
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