Hemoglobin induction in mouse macrophages

Hemoglobin induction in mouse macrophages
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DOI:
10.1073/pnas.96.12.6643
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发表时间:
1999-06-08
影响因子:
11.1
通讯作者:
Stamler, JS
Stamler, JS
中科院分区:
综合性期刊1区
文献类型:
--
作者:
Liu, LM;Zeng, M;Stamler, JS

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血红蛋白仅参与氧气和二氧化碳的运输的常见看法受到最近一氧化氮(NO)研究的挑战。这些研究表明,原始细菌黄素血红蛋白的功能是酶促消耗NO(以保护免受亚硝化应激),而哺乳动物血红蛋白的功能是递送NO(从而使呼吸循环中的氧气递送最大化)。在这里,我们报告,小鼠巨噬细胞刺激产生NO与脂多糖和干扰素-γ表达β(次要)血红蛋白亚基,NO的消耗,但是,不增加细胞因子或血红蛋白的表达。这些数据表明,在哺乳动物细胞中的珠蛋白的替代功能,他们挑战的主流观点,α和β-珠蛋白基因的表达总是平衡和协调。
The common perception that hemoglobin is involved solely in the transport of oxygen and carbon dioxide has been challenged by recent studies with nitric oxide (NO), These studies have shown that the primordial bacterial flavohemoglobin functions to consume NO enzymatically (to protect from nitrosative stress), whereas mammalian hemoglobin functions to deliver NO (thus maximizing oxygen delivery in the respiratory cycle). Here we report that murine macrophages stimulated to produce NO with lipopolysaccharide and interferon-gamma express the beta(minor) hemoglobin subunit, Consumption of NO, however, was not increased by cytokines or by hemoglobin expression. These data suggest alternative functions for globins in mammalian cells, and they challenge the prevailing view that the expression of alpha- and beta-globin genes is always balanced and coordinated.