摘要
背景:巨噬细胞对环境刺激起极化或激活作用,这是机体正常免疫应答的重要过程。同时,巨噬细胞过度活化会引起自身免疫性疾病。因此,防止巨噬细胞过度激活以维持正常的免疫应答是至关重要的。精氨酸酶1(-1)通过调节可用精氨酸的免疫响应的协调起着至关重要的作用。 目的:了解Arg-1调控机制。 方法:实时荧光定量PCR和Western blot分析用于检查从VEGFR1删除和VEGFR1 TK缺陷骨髓巨噬细胞表达Arg-1水平(bmdms)。 结果:VEGFR1介导的信号转导抑制IL-4诱导的Arg-1表达。删除VEGFR1升高导致Arg-1表达VEGFR1酪氨酸激酶域的抑制所需。每三个配体VEGFR1、VEGF-A、VEGF-B和PIGF,介导抑制的相似程度。 结论:我们的研究结果发现VEGFR1避免在精氨酸酶1的表达可能保持适当的先天免疫反应信号的一种新的功能。
关键词: 血管内皮生长因子受体1(VEGFR1)、白细胞介素4(IL-4),精氨酸酶1(-1),巨噬细胞,免疫反应。
Current Molecular Medicine
Title:VEGFR1 Signaling Regulates IL-4-Mediated Arginase 1 Expression in Macrophages
Volume: 17 Issue: 4
关键词: 血管内皮生长因子受体1(VEGFR1)、白细胞介素4(IL-4),精氨酸酶1(-1),巨噬细胞,免疫反应。
摘要: Background: Macrophages undergo polarization or activation in response to environmental stimuli, an essential process for proper immune response. Meanwhile, excessive activation of macrophages causes autoimmune diseases. It is therefore crucial to prevent over-activation of macrophage in order to maintain the proper immune response. Arginase 1 (Arg-1) plays a critical role in coordinating the immune response by regulating availability of arginine.
Objective: To understand the mechanism of Arg-1 regulation.
Methods: Real-time PCR and Western Blot analysis were utilized to examine the Arg-1 levels expressed from the VEGFR1-deleted and VEGFR1-TK-deficient bone marrowderived macrophages (BMDMs).
Results: The VEGFR1-mediated signaling suppressed IL-4-induced Arg-1 expression. Deletion of VEGFR1 resulted in elevated Arg-1 expression and the tyrosine kinase domain of VEGFR1 was required for the suppression. Each of three ligands of VEGFR1, VEGF-A, VEGF-B and PIGF, mediated the inhibition to the similar degree.
Conclusion: Our findings identified a novel function of the VEGFR1 signaling in avoiding over-expression of Arginase 1 potentially to maintain the proper innate immune response.
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Cite this article as:
VEGFR1 Signaling Regulates IL-4-Mediated Arginase 1 Expression in Macrophages, Current Molecular Medicine 2017; 17 (4) . https://dx.doi.org/10.2174/1566524017666171106114537
DOI https://dx.doi.org/10.2174/1566524017666171106114537 |
Print ISSN 1566-5240 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5666 |
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