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Pathophysiology of ANCA-associated small vessel vasculitis.抗中性粒细胞胞质抗体相关性小血管血管炎的病理生理学。
Curr Rheumatol Rep. 2010 Dec;12(6):399-405. doi: 10.1007/s11926-010-0138-6.
2
Inhibitory influence of protease-activated receptor 2 and E-prostanoid receptor stimulants in lipopolysaccharide models of acute airway inflammation.蛋白酶激活受体 2 和 E 类前列腺素受体兴奋剂对脂多糖诱导的急性气道炎症模型的抑制作用。
J Pharmacol Exp Ther. 2010 Nov;335(2):424-33. doi: 10.1124/jpet.109.163253. Epub 2010 Aug 5.
3
S100A8 and S100A9 inhibit neutrophil oxidative metabolism in-vitro: involvement of adenosine metabolites.S100A8 和 S100A9 体外抑制中性粒细胞氧化代谢：涉及腺嘌呤代谢物。
Free Radic Res. 2010 Apr;44(4):389-96. doi: 10.3109/10715760903431434.
4
Involvement of proteinase-activated receptors 1 and 2 in spreading and phagocytosis by murine adherent peritoneal cells: modulation by the C-terminal of S100A9 protein.蛋白水解酶激活受体 1 和 2 参与鼠黏附性腹膜细胞的扩散和吞噬作用：S100A9 蛋白 C 端的调节作用。
Eur J Pharmacol. 2010 Feb 25;628(1-3):240-6. doi: 10.1016/j.ejphar.2009.11.033. Epub 2009 Nov 24.
5
Novel signaling interactions between proteinase-activated receptor 2 and Toll-like receptors in vitro and in vivo.蛋白水解酶激活受体 2 与 Toll 样受体在体外和体内的新型信号相互作用。
Mucosal Immunol. 2010 Jan;3(1):29-39. doi: 10.1038/mi.2009.120. Epub 2009 Oct 28.
6
Protease-activated receptor 2-mediated protection of myocardial ischemia-reperfusion injury: role of transient receptor potential vanilloid receptors.蛋白酶激活受体2介导的心肌缺血再灌注损伤保护作用：瞬时受体电位香草酸受体的作用
Am J Physiol Regul Integr Comp Physiol. 2009 Dec;297(6):R1681-90. doi: 10.1152/ajpregu.90746.2008. Epub 2009 Oct 7.
7
The oral microbial consortium's interaction with the periodontal innate defense system.口腔微生物群落与牙周天然防御系统的相互作用。
DNA Cell Biol. 2009 Aug;28(8):389-95. doi: 10.1089/dna.2009.0864.
8
Suppression of inflammation in rat autoimmune myocarditis by S100A8/A9 through modulation of the proinflammatory cytokine network.S100A8/A9通过调节促炎细胞因子网络抑制大鼠自身免疫性心肌炎中的炎症反应。
Eur J Heart Fail. 2009 Mar;11(3):229-37. doi: 10.1093/eurjhf/hfn049. Epub 2009 Jan 16.
9
S-nitrosylated S100A8: novel anti-inflammatory properties.S-亚硝基化的S100A8：新型抗炎特性。
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10
Inhibiting protease-activated receptor 4 limits myocardial ischemia/reperfusion injury in rat hearts by unmasking adenosine signaling.抑制蛋白酶激活受体4通过揭示腺苷信号来限制大鼠心脏的心肌缺血/再灌注损伤。
J Pharmacol Exp Ther. 2008 Mar;324(3):1045-54. doi: 10.1124/jpet.107.133595. Epub 2007 Nov 30.

S100A8 和 S100A9 对中性粒细胞氧化代谢的下调作用：蛋白酶激活受体-2 的影响。

The down regulation of neutrophil oxidative metabolism by S100A8 and S100A9: implication of the protease-activated receptor-2.

机构信息

Department of Oral Medicine and Diagnostic Sciences, College of Dentistry University of Illinois at Chicago, United States.

出版信息

Mol Immunol. 2012 Feb;50(1-2):42-8. doi: 10.1016/j.molimm.2011.12.001. Epub 2011 Dec 26.

DOI:10.1016/j.molimm.2011.12.001
PMID:22204866
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3288784/
Abstract

S100A8 and S100A9 regulate polymorphonuclear neutrophils (PMNs) recruitment and represent 40% of PMN cytosolic protein weight. We have shown that S100A8/S100A9 inhibit PMN oxidative metabolism. The present study was designed to elucidate the mechanisms of this anti-oxidative effect. We hypothesized that the protease activated receptor-2 (PAR-2) played a role in the down-regulation of PMN oxidative metabolism by S100A8/S100A9. Freshly isolated PMNs were tested for their ability to oxidize dichlorofluorescin-diacetate. Functional inhibition of PAR-2 with ENMD-1068, the pepducin P2pal-21 or an antibody directed at PAR-2 cleavage/activation site, resulted in a significant inhibition of S100A8 and S100A9 anti-oxidative effect. Conversely, the controlled activation of PAR-2 potentiated S100 anti-oxidative effect. Taken together, the data indicate that the anti-oxidative effect of S100A8/A9 is initiated by PAR-2 activation. S100A8/S100A9 may therefore dampen inflammation without interfering with its initial strength. This finding opens translational possibilities to limit deleterious PMN activation with a dual PAR-2/S100 strategy.

摘要

S100A8 和 S100A9 调节多形核粒细胞 (PMN) 的募集，占 PMN 胞质蛋白重量的 40%。我们已经表明，S100A8/S100A9 抑制 PMN 的氧化代谢。本研究旨在阐明这种抗氧化作用的机制。我们假设蛋白酶激活受体-2 (PAR-2) 在 S100A8/S100A9 下调 PMN 氧化代谢中发挥作用。新鲜分离的 PMN 被检测其氧化二氯荧光素二乙酸酯的能力。用 ENMD-1068、肽 P2pal-21 或针对 PAR-2 切割/激活位点的抗体功能抑制 PAR-2，导致 S100A8 和 S100A9 的抗氧化作用显著抑制。相反，PAR-2 的受控激活增强了 S100 的抗氧化作用。总之，这些数据表明 S100A8/A9 的抗氧化作用是由 PAR-2 激活引发的。S100A8/S100A9 因此可能在不干扰其初始强度的情况下抑制炎症。这一发现为采用双重 PAR-2/S100 策略限制有害 PMN 激活提供了转化的可能性。