脂蛋白E缺乏导致脏巨细胞偏向M1表型,从而增加铁含量

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Meng-Qi Shen^1,2, Qian Guo³, Wei Li¹

¹Institute of Translational and Precision Medicine, Nantong University, Nantong, Jiangsu, China.

Genes and immunity

|August 5, 2024

概括

在小鼠中,阿波利波蛋白E (ApoE) 缺乏会改变脏巨细胞的功能,增加铁含量并促进M1亲炎性表型. 这表明ApoE对于维持铁平衡和巨细胞两极分化至关重要.

科学领域:

免疫学免疫学免疫学
血液学血液学血液学
代谢途径代谢途径

背景情况:

脂蛋白E (ApoE) 对于系统性铁平衡至关重要.
巨细胞,特别是脏巨细胞 (SM),是哺乳动物处理铁的关键参与者.
ApoE对SM功能亚型和铁代谢的影响在很大程度上仍未被探索.

研究的目的:

调查ApoE缺乏 (ApoE-/-) 对脏巨细胞两极分化的影响.
确定ApoE缺乏如何影响SM中的铁含量和处理.
阐明这些变化的潜在机制.

主要方法:

在ApoE-/-小鼠中对M1和M2巨细胞极化基因表达标记物的比较分析.
量化铁含量和表达关键的铁相关蛋白质 (ferritin,TfR1,IRP1,HO-1,Fpn1) 在脏和SM.
在28周的老鼠中进行评估.

主要成果:

在SM中,ApoE缺陷显著上调M1标志物 (CD86,IL-1β,IL-6,IL-12,TNF-α,iNOS) 和下调M2标志物 (CD206,Arg-1,IL-10,Ym-1).
ApoE缺乏导致铁含量增加,费里丁,TfR1,IRP1和HO-1表达,以及和/或SM中的Fpn1表达减少.
这些变化在28周大的小鼠中观察到.

结论:

ApoE 缺乏促使脏巨细胞偏向M1表型.
在ApoE-/-小鼠中增加的铁积累归因于铁吸收增加 (通过TfR/IRPs) 和铁释放减少 (通过Fpn1).
ApoE在调节脏巨细胞两极分化和铁代谢方面发挥着重要作用.

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