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首页> 外文期刊>Journal of Cellular Physiology >Nitric oxide induces dose-dependent CA(2+) transients and causes temporal morphological hyperpolarization in human neutrophils.
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Nitric oxide induces dose-dependent CA(2+) transients and causes temporal morphological hyperpolarization in human neutrophils.

机译：一氧化氮产生剂量依赖性CA (2 +)瞬变,导致颞形态在人类中性粒细胞超极化。

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We exposed adherent neutrophils to the nitric oxide (NO)-radical donors S-nitroso-N-acetylpenicillamine (SNAP), S-nitrosoglutathione (GSNO), and sodium nitroprusside (SNP) to study the role of NO in morphology and Ca(2+) signaling. Parallel to video imaging of cell morphology and migration in neutrophils, changes in intracellular free Ca(2+) ([Ca(2+)](i)) were assessed by ratio imaging of Fura-2. NO induced a rapid and persistent morphological hyperpolarization followed by migrational arrest that usually lasted throughout the 10-min experiments. Addition of 0.5-800 microM SNAP caused concentration-dependent elevation of [Ca(2+)](i) with an optimal effect at 50 microM. This was probably induced by NO itself, because no change in [Ca(2+)](i) was observed after treatment with NO donor byproducts, i.e. D-penicillamine, glutathione, or potassium cyanide. Increasing doses of SNAP (>/=200 microM) attenuated the Ca(2+) response to the soluble chemotactic stimulus formyl-methionyl-leucyl-phenylalanine (fMLP), and both NO- and fMLP-induced Ca(2+) transients were abolished at 800 microM SNAP or more. In kinetic studies of fluorescently labeled actin cytoskeleton, NO markedly reduced the F-actin content and profoundly increased cell area. Immunoblotting to investigate the formation of nitrotyrosine residues in cells exposed to NO donors did not imply nitrosylation, nor could we mimic the effects of NO with the cell permeant form of cGMP, i.e., 8-Br-cGMP. Hence these processes were probably not the principal NO targets. In summary, NO donors initially increased neutrophil morphological alterations, presumably due to an increase in [Ca(2+)](i), and thereafter inhibited such shape changes. Our observations demonstrate that the effects of NO donors are important for regulation of cellular signaling, i.e., Ca(2+) homeostasis, and also affect cell migration, e.g., through effects on F-actin turnover. Our results are discussed in relation to the complex mechanisms that govern basic cell shape changes, required for migration. Copyright 2000 Wiley-Liss, Inc.
机译：我们暴露附着氮中性粒细胞氧化(NO)激进的捐助者S-nitroso-N-acetylpenicillamine(临时)S-nitrosoglutathione (GSNO)和钠硝普酸(SNP)研究中没有的作用形态和Ca(2 +)信号。视频成像的细胞形态和迁移中性粒细胞,改变细胞内自由钙(2 +)(Ca(2 +))((我)被比成像评估Fura-2。形态超极化紧随其后迁徙逮捕,通常持续了整个10分钟的实验。microM吸附引起的浓度海拔(Ca(2 +))(我)一个最优的效果在50 microM。本身,因为没有变化(Ca (2 +)) (i)观察治疗后没有捐赠者副产品,例如D-penicillamine、谷胱甘肽或氰化钾。(> / = 200 microM)减毒Ca(2 +)反应溶性趋化现象的刺激formyl-methionyl-leucyl-phenylalanine (fMLP)不——和fMLP-induced Ca(2 +)瞬变废除800 microM吸附或更多。荧光标记肌动蛋白的研究细胞骨架,没有明显减少了f -肌动蛋白内容和深刻的增加细胞区域。免疫印迹调查的形成硝基酪氨酸残基在细胞暴露在不捐助者不意味着亚硝基化,我们也不可能模仿的影响没有细胞渗透的形式的cGMP,即8-Br-cGMP。流程可能不是校长目标。增加中性粒细胞形态改变,大概是由于增加(Ca(2 +))(我),和此后抑制这种形状的变化。观测表明,任何的影响捐赠者对调节细胞很重要信号,即Ca(2 +)体内平衡,和也影响细胞迁移,例如,通过影响f -肌动蛋白营业额。关系管理的复杂机制基本细胞形状变化,需要迁移。版权2000 Wiley-Liss公司。

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