• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>Journal of Cerebral Blood Flow Metabolism >The translational repressor eIF4E-binding protein 2 (4E-BP2) correlates with selective delayed neuronal death after ischemia
【2h】

The translational repressor eIF4E-binding protein 2 (4E-BP2) correlates with selective delayed neuronal death after ischemia

机译：翻译抑制因子eIF4E结合蛋白2（4E-BP2）与局部缺血后选择性神经元死亡相关

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Transient brain ischemia induces an inhibition of translational rates and causes delayed neuronal death in selective regions and cognitive deficits, whereas these effects do not occur in resistant areas. The translational repressor eukaryotic initiation factor (eIF) 4E-binding protein-2 (4E-BP2) specifically binds to eIF4E and is critical in the control of protein synthesis. To link neuronal death to translation inhibition, we study the eIF4E association with 4E-BP2 under ischemia reperfusion in a rat model of transient forebrain ischemia. Upon reperfusion, a selective neuronal apoptosis in the hippocampal cornu ammonis 1 (CA1) region was induced, while it did not occur in the cerebral cortex. Confocal microscopy analysis showed a decrease in 4E-BP2/eIF4E colocalization in resistant cortical neurons after reperfusion. In contrast, in vulnerable CA1 neurons, 4E-BP2 remains associated to eIF4E with a higher degree of 4E-BP2/eIF4E colocalization and translation inhibition. Furthermore, the binding of a 4E-BP2 peptide to eIF4E induced neuronal apoptosis in the CA1 region. Finally, pharmacological-induced protection of CA1 neurons inhibited neuronal apoptosis, decreased 4E-BP2/eIF4E association, and recovered translation. These findings documented specific changes in 4E-BP2/eIF4E association during ischemic reperfusion, linking the translation inhibition to selective neuronal death, and identifying 4E-BP2 as a novel target for protection of vulnerable neurons in ischemic injury.
机译：短暂性脑缺血会抑制翻译速率，并在选择性区域和认知缺陷中引起延迟的神经元死亡，而这些作用在抵抗性区域中不会发生。翻译阻抑物真核起始因子（eIF）4E结合蛋白2（4E-BP2）与eIF4E特异性结合，在控制蛋白合成中至关重要。为了将神经元死亡与翻译抑制联系起来，我们在短暂性前脑缺血的大鼠模型中研究了缺血再灌注下eIF4E与4E-BP2的关系。再灌注后，诱导海马角膜氨氮1（CA1）区的选择性神经元凋亡，而在大脑皮层中没有发生。共聚焦显微镜分析显示抗性皮层神经元再灌注后4E-BP2 / eIF4E共定位减少。相反，在易受攻击的CA1神经元中，4E-BP2仍与eIF4E相关，并具有较高程度的4E-BP2 / eIF4E共定位和翻译抑制作用。此外，4E-BP2肽与eIF4E的结合在CA1区诱导了神经元凋亡。最后，药理学诱导的CA1神经元保护作用抑制神经元凋亡，降低4E-BP2 / eIF4E关联并恢复翻译。这些发现记录了缺血再灌注过程中4E-BP2 / eIF4E关联的特定变化，将翻译抑制与选择性神经元死亡联系在一起，并将4E-BP2鉴定为在缺血性损伤中保护脆弱神经元的新靶标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

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