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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung
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Essential role of nitric oxide in VEGF-induced, asthma-like angiogenic, inflammatory, mucus, and physiologic responses in the lung

机译：一氧化氮在VEGF诱导的哮喘样血管生成，炎症，黏液和肺部生理反应中的重要作用

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摘要

VEGF, nitric oxide (NO), inflammation, and vascular- and extravascular remodeling coexist in asthma and other disorders. In these responses, VEGF regulates angiogenesis. VEGF also induces inflammation and remodeling. The mechanisms of the latter responses have not been defined, however. We hypothesized that VEGF-induces extravascular tissue responses via NO-dependent mechanisms. To evaluate this hypothesis, we compared the effects of transgenic VEGF(165) in lungs from normal mice, mice treated with pan-NO synthase (NOS) or endothelial NOS (eNOS) inhibitors, and mice with null mutations of inducible NOS (iNOS) or eNOS. These studies demonstrate that VEGF selectively stimulates eNOS and NOS. They also demonstrate that VEGF induces pulmonary alterations via NO-dependent and -independent mechanisms with angiogenesis, edema, mucus metaplasia, airway hyperresponsiveness, lymphocyte accumulation, dendritic cell hyperplasia and S-nitrosoglutathione reductase stimulation being NO-dependent and dendritic cell activation being NO-independent. Furthermore, they demonstrate that eNOS and NOS both contribute to these responses. NO/NOS-based interventions may be therapeutic in VEGF-driven inflammation and remodeling.
机译：在哮喘和其他疾病中，VEGF，一氧化氮（NO），炎症以及血管和血管外重构共存。在这些反应中，VEGF调节血管生成。 VEGF还诱导炎症和重塑。但是，尚未定义后一种响应的机制。我们假设VEGF通过NO依赖性机制诱导血管外组织反应。为了评估该假设，我们比较了正常小鼠，经pan-NO合酶（NOS）或内皮型NOS（eNOS）抑制剂治疗的小鼠以及具有诱导型NOS（iNOS）无效突变的小鼠的肺中转基因VEGF（165）的作用。或eNOS。这些研究表明，VEGF选择性刺激eNOS和NOS。他们还证明，VEGF通过NO依赖性和非依赖性机制诱导肺部改变，其中血管生成，水肿，粘液化生，气道高反应性，淋巴细胞蓄积，树突状细胞增生和S-亚硝基谷胱甘肽还原酶刺激为NO依赖性，树突状细胞活化为NO-独立。此外，他们证明eNOS和NOS均有助于这些反应。基于NO / NOS的干预措施可能对VEGF驱动的炎症和重塑具有治疗作用。

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