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首页> 外文期刊>Cellular Signalling >CSF-1 receptor signalling is governed by pre-requisite EHD1 mediated receptor display on the macrophage cell surface
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CSF-1 receptor signalling is governed by pre-requisite EHD1 mediated receptor display on the macrophage cell surface

机译：CSF-1受体信号转导受巨噬细胞表面上必要的EHD1介导的受体显示控制

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摘要

Colony stimulating factor-1 receptor (CSF-1R), a receptor tyrosine kinase (RTK), is the master regulator of macrophage biology. CSF-1 can bind CSF-1R resulting in receptor activation and signalling essential for macrophage functions such as proliferation, differentiation, survival, polarization, phagocytosis, cytokine secretion, and motility. CSF-1R activation can only occur after the receptor is presented on the macrophage cell surface. This process is reliant upon the underlying macrophage receptor trafficking machinery. However, the mechanistic details governing this process are incompletely understood. C-terminal Eps15 Homology Domain-containing (EHD) proteins have recently emerged as key regulators of receptor trafficking but have not yet been studied in the context of macrophage CSF-1R signalling. In this manuscript, we utilize primary bone-marrow derived macrophages (BMDMs) to reveal a novel function of EHD1 as a regulator of CSF-1R abundance on the cell surface. We report that EHD1-knockout (EHD1-KO) macrophages cell surface and total CSF-1R levels are significantly decreased. The decline in CSF-1R levels corresponds with reduced downstream macrophage functions such as cell proliferation, migration, and spreading. In EHD1-K0 macrophages, transport of newly synthesized CSF-1R to the macrophage cell surface was reduced and was associated with the shunting of the receptor to the lysosome, which resulted in receptor degradation. These findings reveal a novel and functionally important role for EHD1 in governing CSF-1R signalling via regulation of anterograde transport of CSF-1R to the macrophage cell surface. (C) 2016 Elsevier Inc. All rights reserved.
机译：集落刺激因子-1受体（CSF-1R），酪氨酸激酶（RTK）受体，是巨噬细胞生物学的主要调节剂。 CSF-1可以结合CSF-1R，从而导致受体活化和巨噬细胞功能（如增殖，分化，存活，极化，吞噬作用，细胞因子分泌和运动）所必需的信号转导。 CSF-1R激活只能在巨噬细胞表面上出现受体后发生。这个过程依赖于潜在的巨噬细胞受体运输机制。但是，控制该过程的机械细节尚未完全理解。 C端包含Eps15同源域的蛋白（EHD）最近已成为受体运输的关键调节因子，但尚未在巨噬细胞CSF-1R信号传导方面进行研究。在此手稿中，我们利用原代骨髓来源的巨噬细胞（BMDMs）揭示EHD1作为细胞表面CSF-1R丰度调节剂的新功能。我们报告说，EHD1-基因敲除（EHD1-KO）巨噬细胞表面和总CSF-1R水平明显降低。 CSF-1R水平的下降与下游巨噬细胞功能（例如细胞增殖，迁移和扩散）减少相对应。在EHD1-K0巨噬细胞中，新合成的CSF-1R向巨噬细胞表面的转运减少，并且与受体与溶酶体的分流有关，从而导致受体降解。这些发现揭示了EHD1在通过调节CSF-1R向巨噬细胞细胞表面的顺行转运来调控CSF-1R信号传导中的新颖且功能上重要的作用。 （C）2016 Elsevier Inc.保留所有权利。

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