PRMT2 silencing regulates macrophage polarization through activation of STAT1 or inhibition of STAT6.

IF 2.9 4区 医学 Q3 IMMUNOLOGY
Ting Liu, Yinjiao Li, Muqiu Xu, Hongjun Huang, Yan Luo
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引用次数: 0

Abstract

Background: Macrophages play significant roles in innate immune responses and are heterogeneous cells that can be polarized into M1 or M2 phenotypes. PRMT2 is one of the type I protein arginine methyltransferases involved in inflammation. However, the role of PRMT2 in M1/M2 macrophage polarization remains unclear. Our study revealed the effect and mechanism of PRMT2 in macrophage polarization.

Methods: Bone marrow-derived macrophages (BMDMs) were polarized to M1 or M2 state by LPS plus murine recombinant interferon-γ (IFN-γ) or interleukin-4 (IL-4). Quantitative polymerase chain reaction (qPCR), western blot and flow cytometry (FCM) assay were performed and analyzed markers and signaling pathways of macrophage polarization.

Results: We found that PRMT2 was obviously upregulated in LPS/IFN-γ-induced M1 macrophages, but it was little changed in IL-4-induced M2 macrophages. Furthermore, PRMT2 konckdown increased the expression of M1 macrophages markers through activation of STAT1 and decreased the expression of M2 macrophages markers through inhibition of STAT6.

Conclusions: PRMT2 silencing modulates macrophage polarization by activating STAT1 to promote M1 and inhibiting STAT6 to attenuate the M2 state.

PRMT2 沉默通过激活 STAT1 或抑制 STAT6 来调节巨噬细胞的极化。
背景:巨噬细胞在先天性免疫反应中发挥着重要作用,是一种可极化为 M1 或 M2 表型的异型细胞。PRMT2 是参与炎症的 I 型蛋白精氨酸甲基转移酶之一。然而,PRMT2 在巨噬细胞 M1/M2 极化中的作用仍不清楚。我们的研究揭示了PRMT2在巨噬细胞极化中的作用和机制:方法:用 LPS 加小鼠重组干扰素-γ(IFN-γ)或白细胞介素-4(IL-4)将骨髓源性巨噬细胞(BMDMs)极化为 M1 或 M2 状态。对巨噬细胞极化的标志物和信号通路进行了定量聚合酶链反应(qPCR)、Western印迹和流式细胞术(FCM)分析:结果:我们发现,PRMT2在LPS/IFN-γ诱导的M1巨噬细胞中明显上调,但在IL-4诱导的M2巨噬细胞中变化不大。此外,PRMT2 konckdown通过激活STAT1增加M1巨噬细胞标志物的表达,通过抑制STAT6减少M2巨噬细胞标志物的表达:结论:PRMT2沉默通过激活STAT1促进M1和抑制STAT6减轻M2状态来调节巨噬细胞极化。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
BMC Immunology
BMC Immunology 医学-免疫学
CiteScore
5.50
自引率
0.00%
发文量
54
审稿时长
1 months
期刊介绍: BMC Immunology is an open access journal publishing original peer-reviewed research articles in molecular, cellular, tissue-level, organismal, functional, and developmental aspects of the immune system as well as clinical studies and animal models of human diseases.
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