Nitric oxide and zinc homeostasis in acute lung injury.
Nitric oxide and zinc homeostasis in acute lung injury.
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DOI：
10.1513/pats.200501-007ac
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发表时间：
2005-01-01
期刊：
影响因子：
--
通讯作者：
Pitt, Bruce R
中科院分区：
文献类型：
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作者：
St Croix, Claudette M;Leelavaninchkul, Karanee;Pitt, Bruce R
在已知的影响急性肺损伤敏感性的小分子中，锌和一氧化氮可能是独特的，因为它们相互依赖，具有细胞保护或损伤的双重能力。一氧化氮和锌似乎通过细胞内信号通路连接，涉及金属硫蛋白的s -亚硝化作用，金属硫蛋白本身是一种已知的重要诱导基因产物，可能改变肺损伤。在本文中，我们总结了近年来利用遗传和荧光光学成像技术的研究成果：(1)证明金属硫蛋白的s -亚硝化影响完整肺内皮细胞内锌的稳态；(2)揭示了该通路在高氧和lps诱导的损伤中的保护作用。
Among putative small molecules that affect sensitivity to acute lung injury, zinc and nitric oxide are potentially unique by virtue of their interdependence and dual capacities to be cytoprotective or injurious. Nitric oxide and zinc appear to be linked via an intracellular signaling pathway involving S-nitrosation of metallothoinein--itself a small protein known to be an important inducible gene product that may modify lung injury. In the present article, we summarize recent efforts using genetic and fluorescence optical imaging techniques to: (1) demonstrate that S-nitrosation of metallothionein affects intracellular zinc homeostasis in intact pulmonary endothelial cells; and (2) reveal a protective role for this pathway in hyperoxic and LPS-induced injury.