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中性粒细胞对甲酰甲硫氨酰-亮氨酰-苯丙氨酸诱导的分泌囊泡动员和NADPH氧化酶激活的控制:配体-受体复合物与细胞骨架结合的作用

Neutrophil control of formylmethionyl-leucyl-phenylalanine induced mobilization of secretory vesicles and NADPH-oxidase activation: effect of an association of the ligand-receptor complex to the cytoskeleton.

作者信息

Lundqvist H, Gustafsson M, Johansson A, Särndahl E, Dahlgren C

机构信息

Department of Medical Microbiology and Immunology, University of Göteborg, Sweden.

出版信息

Biochim Biophys Acta. 1994 Oct 20;1224(1):43-50. doi: 10.1016/0167-4889(94)90111-2.

DOI:10.1016/0167-4889(94)90111-2
PMID:7948041
Abstract

The stimulus formylmethionyl-leucyl-phenylalanine (FMLP) interacts with neutrophils and generates signal(s) in the cells that induces mobilization of the secretory vesicles as well as activation of the superoxide anion/hydrogen peroxide generating NADPH-oxidase. Binding, at 15 degrees C, of FMLP to its neutrophil surface receptor is followed by an association of the ligand-receptor complex to the cell cytoskeleton, and this association occurs concomitant with a desensitization of the cells with respect to activation of the NADPH-oxidase. Other stimuli can still activate the oxidase (in fact even induce a primed response), indicating that the observed phenomenon is stimulus specific and could not be accounted for by an effect on the oxidase itself, but rather that the association of the ligand-receptor complex to the cytoskeleton eliminates the capacity of the complex to generate the signal(s) that activates the NADPH-oxidase. The cytoskeleton associated ligand-receptor complex generates, however, the signal(s) responsible for mobilization of the secretory vesicles, to the plasma membrane, and this mobilization occurs without any increase in the intracellular concentration of free Ca2+.

摘要

刺激物甲酰甲硫氨酰 - 亮氨酰 - 苯丙氨酸(FMLP)与中性粒细胞相互作用,并在细胞内产生信号,诱导分泌囊泡的动员以及超氧阴离子/过氧化氢生成型NADPH氧化酶的激活。在15℃下,FMLP与其中性粒细胞表面受体结合后,配体 - 受体复合物会与细胞骨架结合,并且这种结合与细胞对NADPH氧化酶激活的脱敏同时发生。其他刺激仍可激活氧化酶(实际上甚至可诱导预激发反应),这表明观察到的现象是刺激特异性的,不能用对氧化酶本身的影响来解释,而是配体 - 受体复合物与细胞骨架的结合消除了复合物产生激活NADPH氧化酶信号的能力。然而,与细胞骨架相关的配体 - 受体复合物会产生负责将分泌囊泡动员到质膜的信号,并且这种动员在细胞内游离Ca2 +浓度没有任何增加的情况下发生。

相似文献

1
Neutrophil control of formylmethionyl-leucyl-phenylalanine induced mobilization of secretory vesicles and NADPH-oxidase activation: effect of an association of the ligand-receptor complex to the cytoskeleton.中性粒细胞对甲酰甲硫氨酰-亮氨酰-苯丙氨酸诱导的分泌囊泡动员和NADPH氧化酶激活的控制:配体-受体复合物与细胞骨架结合的作用
Biochim Biophys Acta. 1994 Oct 20;1224(1):43-50. doi: 10.1016/0167-4889(94)90111-2.
2
Desensitization of formyl peptide receptors is abolished in calcium ionophore-primed neutrophils: an association of the ligand-receptor complex to the cytoskeleton is not required for a rapid termination of the NADPH-oxidase response.钙离子载体预处理的中性粒细胞中,甲酰肽受体脱敏作用消失:NADPH氧化酶反应的快速终止并不需要配体-受体复合物与细胞骨架结合。
J Immunol. 1998 Mar 1;160(5):2463-8.
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Chemoattractant-induced NADPH oxidase activity in human monocytes is terminated without any association of receptor-ligand complex to cytoskeleton.趋化因子诱导的人类单核细胞中的NADPH氧化酶活性被终止,且受体-配体复合物与细胞骨架无任何关联。
Inflammation. 1995 Apr;19(2):179-91. doi: 10.1007/BF01534460.
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Desensitization of the fMLP-induced NADPH-oxidase response in human neutrophils is lacking in okadaic acid-treated cells.在经冈田酸处理的细胞中,人中性粒细胞中fMLP诱导的NADPH氧化酶反应缺乏脱敏现象。
J Leukoc Biol. 1997 Jun;61(6):753-8. doi: 10.1002/jlb.61.6.753.
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Escherichia coli-induced activation of neutrophil NADPH-oxidase: lipopolysaccharide and formylated peptides act synergistically to induce release of reactive oxygen metabolites.大肠杆菌诱导的中性粒细胞NADPH氧化酶激活:脂多糖和甲酰化肽协同作用诱导活性氧代谢产物的释放。
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Complete dissociation between the activation of phosphoinositide turnover and of NADPH oxidase by formyl-methionyl-leucyl-phenylalanine in human neutrophils depleted of Ca2+ and primed by subthreshold doses of phorbol 12,myristate 13,acetate.在经亚阈值剂量的佛波醇12 -肉豆蔻酸酯13 -乙酸酯预处理且Ca2+耗尽的人中性粒细胞中,甲酰甲硫氨酰亮氨酰苯丙氨酸对磷酸肌醇代谢周转的激活与对NADPH氧化酶的激活完全解离。
Biochem Biophys Res Commun. 1986 Mar 28;135(3):785-94. doi: 10.1016/0006-291x(86)90997-6.
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Subcellular localization and translocation of the receptor for N-formylmethionyl-leucyl-phenylalanine in human neutrophils.人中性粒细胞中N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸受体的亚细胞定位与转运
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J Leukoc Biol. 1991 Mar;49(3):236-44. doi: 10.1002/jlb.49.3.236.

引用本文的文献

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Reactivation of desensitized formyl peptide receptors by platelet activating factor: a novel receptor cross talk mechanism regulating neutrophil superoxide anion production.血小板激活因子使脱敏的甲酰肽受体再激活:调节中性粒细胞超氧化物阴离子产生的新型受体串扰机制。
PLoS One. 2013;8(3):e60169. doi: 10.1371/journal.pone.0060169. Epub 2013 Mar 28.
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The two neutrophil members of the formylpeptide receptor family activate the NADPH-oxidase through signals that differ in sensitivity to a gelsolin derived phosphoinositide-binding peptide.
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BMC Cell Biol. 2004 Dec 29;5(1):50. doi: 10.1186/1471-2121-5-50.
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Cytochalasin B triggers a novel pertussis toxin sensitive pathway in TNF-alpha primed neutrophils.细胞松弛素B在肿瘤坏死因子-α预处理的中性粒细胞中触发一条新的百日咳毒素敏感途径。
BMC Cell Biol. 2004 May 24;5:21. doi: 10.1186/1471-2121-5-21.
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Clin Exp Immunol. 1999 Nov;118(2):253-60. doi: 10.1046/j.1365-2249.1999.01040.x.
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