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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >Nitric Oxide positively regulates Ag (I)-induced Ca(2+) influx and mast cell activation: role of a Nitric Oxide Synthase-independent pathway.
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Nitric Oxide positively regulates Ag (I)-induced Ca(2+) influx and mast cell activation: role of a Nitric Oxide Synthase-independent pathway.

机译：一氧化氮积极调节银（I）诱导的Ca（2+）涌入和肥大细胞激活：一氧化氮合酶独立途径的作用。

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摘要

NO is generated by NOS activity and known to act as a negative regulator of mast cell activation. We reported previously that Ag (I) directly evokes mast cell degranulation and LTC(4) release via Ca(2+) influx through thiol-sensitive, store-independent channels. Here, we report that NO generated independently of NOS activity mediates the store-independent Ca(2+) influx. Exposure of mast cells to Ag (I) resulted in increased intracellular NO levels and NO(2)(-)/NO(3)(-) contents in the extracellular fluid. The NO increase was blocked by NO scavenger Hb and DTT but not by NOS inhibitors such as amino-BH(4) and L-NAME. This NO production occurred independently of the Src family kinase and PI3K activities, both of which were necessary for antigen-induced, NOS-dependent NO production. Hb and DTT reduced Ag (I)-induced beta-hexosaminidase release and LTC(4) release, whereas the NO scavengers and NOS inhibitors augmented antigen-induced mediator release. Moreover, Hb and DTT, but not the NOS inhibitors, abolished the Ag (I)-induced Ca(2+) influx, and none of the drugs blocked CRAC channel activity. Finally, Ag (I)-induced Ca(2+) influx was distinct from LTCC activity in terms of its sensitivities to wortmannin and LTCC antagonists and the effects of Ca(v)1.2 LTCC gene silencing. These data show that NOS-independent NO regulates mast cell activation positively via a unique store-independent Ca(2+) influx pathway. The present findings suggest multiple sources and functions of NO in mast cell biology.
机译：NO是由NOS活性产生的，并已知其作为肥大细胞激活的负调节剂。我们以前报道过，银（I）直接引起肥大细胞脱粒和LTC（4）释放通过Ca（2+）涌入通过硫醇敏感，独立于存储的通道。在这里，我们报告说，独立于NOS活性生成的NO介导了存储独立的Ca（2+）涌入。肥大细胞暴露于Ag（I）导致细胞内NO水平和细胞外液中NO（2）（-）/ NO（3）（-）含量增加。 NO的增加被NO清除剂Hb和DTT阻止，但未被NOS抑制剂（如氨基BH（4）和L-NAME）阻止。这种NO的产生独立于Src家族激酶和PI3K的活性，这对于抗原诱导的，依赖NOS的NO产生都是必需的。血红蛋白和DTT减少Ag（I）诱导的β-己糖胺酶释放和LTC（4）释放，而NO清道夫和NOS抑制剂增加抗原诱导的介质释放。此外，血红蛋白和DTT，但不是NOS抑制剂，废除了Ag（I）诱导的Ca（2+）涌入，并且没有一种药物能阻止CRAC通道活性。最后，就其对渥曼青霉素和LTCC拮抗剂的敏感性以及Ca（v）1.2 LTCC基因沉默的影响而言，Ag（I）诱导的Ca（2+）涌入不同于LTCC活性。这些数据表明，独立于NOS的NO通过唯一的独立于存储的Ca（2+）流入途径积极调节肥大细胞的激活。目前的发现提示肥大细胞生物学中NO的多种来源和功能。

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