• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Short-term modulation of interleukin-1beta signaling by hyperoxia: uncoupling of IkappaB kinase activation and NF-kappaB-dependent gene expression.
【24h】

Short-term modulation of interleukin-1beta signaling by hyperoxia: uncoupling of IkappaB kinase activation and NF-kappaB-dependent gene expression.

机译：高氧对白介素1beta信号的短期调节：IkappaB激酶激活和NF-kappaB依赖性基因表达的解偶联。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

We have been interested in elucidating how simultaneous stimuli modulate inflammation-related signal transduction pathways in lung parenchymal cells. We previously demonstrated that exposing respiratory epithelial cells to 95% oxygen (hyperoxia) synergistically increased tumor necrosis factor-alpha (TNF-alpha)-mediated activation of NF-kappaB and NF-kappaB-dependent gene expression by a mechanism involving increased activation of IkappaB kinase (IKK). Because the signal transduction mechanisms induced by IL-1beta are distinct to that of TNF-alpha, herein we sought to determine whether hyperoxia modulates IL-1beta-dependent signal transduction. In A549 cells, simultaneous treatment with hyperoxia and IL-1beta caused increased activation of IKK, prolonged the degradation of IkappaBalpha, and prolonged the nuclear translocation and DNA binding of NF-kappaB compared with cells treated with IL-1beta alone in room air. Hyperoxia did not affect IL-1beta-dependent degradation of the interleukin receptor-associated kinase differently from treatment with IL-beta alone. In contrast to the effects on the IKK/IkappaBalpha/NF-kappaB pathway, simultaneous treatment with hyperoxia and IL-1beta did not augment NF-kappaB-dependent gene expression compared with treatment with IL-1beta alone. Similar observations were made in a different human respiratory epithelial cell line, BEAS-2B cells. In addition, simultaneous treatment with hyperoxia and IL-1beta caused hyperphosphorlyation of the NF-kappaB p65 subunit compared with treatment with IL-1beta alone. In summary, concomitant treatment of A549 cells with hyperoxia and IL-1beta augments activation of IKK, prolongs degradation of IkappaBalpha, and prolongs nuclear translocation and DNA binding of NF-kappaB. This activation, however, is not coupled to increased expression of NF-kappaB-dependent genes, and the mechanism of this decoupling is not related to decreased phosphorylation of p65.
机译：我们一直对阐明同时刺激如何调节肺实质细胞中炎症相关信号转导途径感兴趣。我们以前证明，呼吸呼吸道上皮细胞暴露于95％的氧气（高氧）会通过涉及增加IkappaB激活的机制协同增加肿瘤坏死因子-α（TNF-alpha）介导的NF-kappaB和NF-kappaB依赖性基因表达的激活。激酶（IKK）。因为IL-1beta诱导的信号转导机制不同于TNF-α，所以在这里我们试图确定高氧是否调节IL-1beta依赖性信号转导。与在室内空气中单独用IL-1beta处理的细胞相比，在A549细胞中，高氧和IL-1beta的同时处理引起IKK的激活增加，延长了IkappaBalpha的降解，并延长了NF-kappaB的核转运和DNA结合。高氧对IL-1β依赖性白介素受体相关激酶的降解与单独使用IL-β的影响不同。与对IKK / IkappaBalpha / NF-kappaB途径的影响相反，与仅用IL-1beta进行治疗相比，同时进行高氧血症和IL-1beta治疗不会增加NF-kappaB依赖性基因表达。在不同的人类呼吸道上皮细胞系BEAS-2B细胞中也得到了类似的观察结果。另外，与仅用IL-1beta治疗相比，同时用高氧和IL-1β治疗引起NF-κBp65亚基的过度磷酸化。总之，高氧血症和IL-1β对A549细胞的伴随治疗可增强IKK的激活，延长IkappaBalpha的降解，并延长核转运和NF-kappaB的DNA结合。但是，这种激活与NF-κB依赖性基因的表达增加无关，并且这种解偶联的机制与p65磷酸化的降低无关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号