Stress response decreases NF-kappaB nuclear translocation and increases I-kappaBalpha expression in A549 cells.
Stress response decreases NF-kappaB nuclear translocation and increases I-kappaBalpha expression in A549 cells.
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应激反应会降低 A549 细胞中 NF-kappaB 核转位并增加 I-kappaBalpha 表达。
DOI：
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发表时间：
1997
影响因子：
15.9
通讯作者：
Jonathan R. Wispé
中科院分区：
文献类型：
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作者：
Hector R. Wong;M. Ryan;Jonathan R. Wispé
应激反应和应激蛋白赋予针对不同形式的细胞和组织损伤的保护，包括急性肺损伤。应激反应可抑制非应激蛋白基因表达，因此转录抑制促炎反应可能是急性肺损伤的保护机制。为了探索这种可能性，我们确定了应激反应对转录因子NF-κ B核转位的影响，NF-κ B是促炎基因表达的重要调节因子。在A549细胞中，应激反应的诱导减少了肿瘤坏死因子-α（TNF-α）介导的NF-κ B核转位。TNF-α通过引起抑制性蛋白I-kappaB α从NF-κ B上解离和I-kappaB α的快速降解来启动NF-κ B核转位。预先诱导应激反应可抑制TNF-α介导的I-κ B α与NF-κ B的解离以及随后的I-κ B α降解。应激反应的诱导也增加了I-κ B α的表达。我们的结论是，应激反应影响NF κ B介导的基因调控由两个独立的机制。应激反应稳定I-κ B α并诱导I-κ B α的表达。这两种效应的复合结果是减少NF-κ B核转位。我们推测应激反应对急性肺损伤的保护作用涉及对I-kappaB/NF-kappaB通路的类似作用。
The stress response and stress proteins confer protection against diverse forms of cellular and tissue injury, including acute lung injury. The stress response can inhibit nonstress protein gene expression, therefore transcriptional inhibition of proinflammatory responses could be a mechanism of protection against acute lung injury. To explore this possibility, we determined the effects of the stress response on nuclear translocation of the transcription factor NF-kappaB, an important regulator of proinflammatory gene expression. In A549 cells induction of the stress response decreased tumor necrosis factor-alpha (TNF-alpha)-mediated NF-kappaB nuclear translocation. TNF-alpha initiates NF-kappaB nuclear translocation by causing dissociation of the inhibitory protein I-kappaBalpha from NF-kappaB and rapid degradation of I-kappaBalpha. Prior induction of the stress response inhibited TNF-alpha-mediated dissociation of I-kappaBalpha from NF-kappaB and subsequent degradation of I-kappaBalpha. Induction of the stress response also increased expression of I-kappaBalpha. We conclude that the stress response affects NFkappaB-mediated gene regulation by two independent mechanisms. The stress response stabilizes I-kappaBalpha and induces expression of I-kappaBalpha. The composite result of these two effects is to decrease NF-kappaB nuclear translocation. We speculate that the protective effect of the stress response against acute lung injury involves a similar effect on the I-kappaB/NF-kappaB pathway.
细胞因子诱导的一氧化氮合酶基因转录被人肝细胞的热休克反应所阻断。
影响因子：
3.8
作者：
deVera,ME;Wong,JM;Zhou,JY;Tzeng,E;Wong,HR;Billiar,TR;Geller,DA
通讯作者：
Geller,DA
DOI：
10.1073/pnas.79.10.3218
发表时间：
1982-01-01
期刊：
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA-BIOLOGICAL SCIENCES
影响因子：
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作者：
LI, GC;WERB, Z
通讯作者：
WERB, Z