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Activation of Adhesion GPCR EMR2/ADGRE2 Induces Macrophage Differentiation and Inflammatory Responses via Gα16/Akt/MAPK/NF-κB Signaling Pathways

机译:粘附GpCR EmR2 / aDGRE2的激活通过Gα16/ akt / mapK / NF-κB信号通路诱导巨噬细胞分化和炎症反应

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摘要

EMR2/ADGRE2 is a human myeloid-restricted adhesion G protein-coupled receptor critically implicated in vibratory urticaria, a rare type of allergy caused by vibration-induced mast cell activation. In addition, EMR2 is also highly expressed by monocyte/macrophages and has been linked to neutrophil migration and activation. Despite these findings, little is known of EMR2-mediated signaling and its role in myeloid biology. In this report, we show that activation of EMR2 via a receptor-specific monoclonal antibody promotes the differentiation of human THP-1 monocytic cell line and induces the expression of pro-inflammatory mediators, including IL-8, TNF-α, and MMP-9. Using specific signaling inhibitors and siRNA knockdowns, biochemical and functional analyses reveal that the EMR2-mediated signaling is initiated by Gα16, followed by the subsequent activation of Akt, extracellular signal-regulated kinase, c-Jun N-terminal kinase, and nuclear factor kappa-light-chain-enhancer of activated B cells. Our results demonstrate a functional role for EMR2 in the differentiation and inflammatory activation of human monocytic cells and provide potential targets for myeloid cell-mediated inflammatory disorders.
机译:EMR2 / ADGRE2是一种人类髓样受限的粘附G蛋白偶联受体,主要参与振动性荨麻疹,这是一种由振动诱导的肥大细胞活化引起的罕见变态反应。此外,EMR2在单核细胞/巨噬细胞中也高度表达,并与嗜中性粒细胞迁移和激活有关。尽管有这些发现,但对EMR2介导的信号传导及其在髓样生物学中的作用了解甚少。在本报告中,我们表明通过受体特异性单克隆抗体激活EMR2可以促进人THP-1单核细胞系的分化并诱导促炎性介质(包括IL-8,TNF-α和MMP- 9。使用特定的信号传导抑制剂和siRNA敲低,生化和功能分析表明EMR2介导的信号传导是由Gα16启动的,随后是Akt,细胞外信号调节激酶,c-Jun N端激酶和核因子kappa的后续活化。 -活化的B细胞的轻链增强子。我们的结果证明了EMR2在人类单核细胞的分化和炎症激活中的功能性作用,并为髓样细胞介导的炎症性疾病提供了潜在的靶标。

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