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神经生长因子促进的小鼠巨噬细胞的功能特性

Functional properties of murine macrophages promoted by nerve growth factor.

作者信息

Susaki Y, Shimizu S, Katakura K, Watanabe N, Kawamoto K, Matsumoto M, Tsudzuki M, Furusaka T, Kitamura Y, Matsuda H

机构信息

Department of Veterinary Clinic, Faculty of Agriculture, Tokyo University of Agriculture and Technology, Japan.

出版信息

Blood. 1996 Dec 15;88(12):4630-7.

PMID:8977255
Abstract

The stimulating effect of nerve growth factor (NGF) on phagocytosis, parasite killing, and interleukin-1beta (IL-1beta) production of murine peritoneal macrophages was assessed. In the presence of various doses of NGF, macrophages showed the increased phagocytosis of both nonspecific hydrophilic microspheres and sheep red blood cells (SRBC) opsonized with anti-SRBC antibodies (Ab) or complement in a dose-dependent manner. NGF also enhanced killing of Leishmania donovani promastigotes by macrophages, and its ability was comparable with that of an optimal dose of recombinant granulocyte-macrophage colony-stimulating factor or recombinant interferon-gamma. The addition of NGF to peritoneal macrophages and monocyte-macrophage J774A.1 cells led to a significant release of IL-1beta in a dose-dependent manner and expression of IL-1beta mRNA. Because pretreatment of peritoneal macrophages and J774A.1 cells with K-252a, a tyrosine kinase inhibitor, completely suppressed these NGF-mediated stimulating effects and p140trk phosphorylation and because flow cytometric analysis with specific Ab against two distinct NGF receptors showed the expression of p140trk, unlike p75LNGFR, on the surface of macrophages, the stimulating activity of NGF to murine macrophages may be mediated through p140trk. Thus, NGF may act as an activator for murine macrophages in the process of inflammatory and immune actions.

摘要

评估了神经生长因子(NGF)对小鼠腹腔巨噬细胞吞噬作用、杀灭寄生虫以及白细胞介素-1β(IL-1β)产生的刺激作用。在存在不同剂量NGF的情况下,巨噬细胞对非特异性亲水性微球以及用抗绵羊红细胞(SRBC)抗体(Ab)或补体调理的绵羊红细胞(SRBC)的吞噬作用呈剂量依赖性增加。NGF还增强了巨噬细胞对杜氏利什曼原虫前鞭毛体的杀伤作用,其能力与最佳剂量的重组粒细胞-巨噬细胞集落刺激因子或重组干扰素-γ相当。向腹腔巨噬细胞和单核巨噬细胞J774A.1细胞中添加NGF导致IL-1β以剂量依赖性方式显著释放并表达IL-1β mRNA。由于用酪氨酸激酶抑制剂K-252a预处理腹腔巨噬细胞和J774A.1细胞可完全抑制这些NGF介导的刺激作用和p140trk磷酸化,并且由于用针对两种不同NGF受体的特异性抗体进行的流式细胞术分析显示巨噬细胞表面表达p140trk,与p75LNGFR不同,NGF对小鼠巨噬细胞的刺激活性可能是通过p140trk介导的。因此,NGF在炎症和免疫作用过程中可能作为小鼠巨噬细胞的激活剂。

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1
Functional properties of murine macrophages promoted by nerve growth factor.神经生长因子促进的小鼠巨噬细胞的功能特性
Blood. 1996 Dec 15;88(12):4630-7.
2
Nerve growth factor prevents apoptosis of rat peritoneal mast cells through the trk proto-oncogene receptor.神经生长因子通过trk原癌基因受体防止大鼠腹膜肥大细胞凋亡。
Blood. 1995 Dec 15;86(12):4638-44.
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Expression of human p140trk receptors in p140trk-deficient, PC12/endothelial cells results in nerve growth factor-induced signal transduction and DNA synthesis.在缺乏p140trk的PC12/内皮细胞中表达人p140trk受体,会导致神经生长因子诱导的信号转导和DNA合成。
J Cell Biochem. 1997 Aug 1;66(2):229-44.
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High affinity nerve growth factor binding displays a faster rate of association than p140trk binding. Implications for multi-subunit polypeptide receptors.高亲和力神经生长因子结合的缔合速率比p140trk结合更快。对多亚基多肽受体的启示。
J Biol Chem. 1994 Mar 4;269(9):6884-91.
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K-252a inhibits nerve growth factor-induced trk proto-oncogene tyrosine phosphorylation and kinase activity.K-252a抑制神经生长因子诱导的trk原癌基因酪氨酸磷酸化和激酶活性。
J Biol Chem. 1992 Jan 5;267(1):13-6.
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Monoamine-activated alpha 2-macroglobulin binds trk receptor and inhibits nerve growth factor-stimulated trk phosphorylation and signal transduction.单胺激活的α2-巨球蛋白结合trk受体并抑制神经生长因子刺激的trk磷酸化和信号转导。
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Induction of nerve growth factor responsiveness in C6-2B glioma cells by expression of trkA proto-oncogene.通过trkA原癌基因的表达诱导C6-2B胶质瘤细胞中神经生长因子反应性
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Nerve growth factor modulates Fc gamma receptor expression on murine macrophage J774A.1 cells.神经生长因子调节小鼠巨噬细胞J774A.1细胞上Fcγ受体的表达。
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p75 and TrkA receptor signaling independently regulate amyloid precursor protein mRNA expression, isoform composition, and protein secretion in PC12 cells.p75和TrkA受体信号通路分别调节PC12细胞中淀粉样前体蛋白的mRNA表达、异构体组成和蛋白质分泌。
J Neurochem. 1998 Aug;71(2):757-66. doi: 10.1046/j.1471-4159.1998.71020757.x.

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