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

中文翻译：

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PRMT2 沉默通过激活 STAT1 或抑制 STAT6 调节巨噬细胞极化

巨噬细胞在先天免疫反应中发挥着重要作用，并且是可以极化为 M1 或 M2 表型的异质细胞。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 M1/M2 巨噬细胞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。LPS 加鼠重组干扰素-γ (IFN-γ) 或白细胞介素-4 (IL-4) 将骨髓源性巨噬细胞 (BMDM) 极化为 M1 或 M2 状态。进行定量聚合酶链反应（qPCR）、蛋白质印迹和流式细胞术（FCM）测定并分析巨噬细胞极化的标志物和信号通路。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，并通过抑制 STAT6 减少 M2 巨噬细胞标志物的表达。PRMT2 沉默通过激活 STAT1 促进 M1 并抑制 STAT6 减弱 M2 状态来调节巨噬细胞极化。