s -亚硝基化S100A8:新型抗炎特性。
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林世善，Raftery M，蔡浩，徐坤，闫文祥，谢海林，Watts RN, Richardson D, Thomas S, Perry M, Geczy CL
s -亚硝基化S100A8:新型抗炎特性。
中华免疫杂志2008 10月15日;181(8):5627-36。
- PubMed ID
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18832721 (PubMed视图］
- 摘要
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S100A8和S100A9在中性粒细胞、活化的巨噬细胞和微血管内皮细胞中高度表达，在炎症过程中分泌。我们早期的研究表明，S100A8是一种强烈的氧化剂清道夫，加上它依赖IL-10在巨噬细胞中表达，我们假设这种蛋白质具有保护作用。s -亚硝基化是一种重要的翻译后修饰，调节NO转运、细胞信号转导和稳态。相对较少的蛋白质是s -亚硝基化的靶点。到目前为止，还没有发现具有no穿梭能力的炎症相关蛋白。我们使用高效液相色谱法和质谱法表明，S100A8和S100A9易于被NO供体s -亚硝基化。s -亚硝基化S100A8 (S100A8- sno)是首选的亚硝基化产物。S100A8中单个Cys残基突变为Ala时，未发生s -亚硝基化。生物素开关试验证实了用NO供体处理的人中性粒细胞中的S100A8-SNO。稳定加合物跨亚硝基化血红蛋白，表明在NO转运中起作用。 S100A8-SNO suppressed mast cell activation by compound 48/80; intravital microscopy was used to demonstrate suppression of leukocyte adhesion and extravasation triggered by compound 48/80 in the rat mesenteric microcirculation. Although S100A8 is induced in macrophages by LPS or IFN-gamma, the combination, which activates inducible NO synthase, did not induce S100A8. Thus, the antimicrobial functions of NO generated under these circumstances would not be compromised by S100A8. Our results suggest that S100A8-SNO may regulate leukocyte-endothelial cell interactions in the microcirculation, and suppression of mast cell-mediated inflammation represents an additional anti-inflammatory property for S100A8.