首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Activation of endoplasmic reticulum stress response following trauma-hemorrhage.
【24h】

Activation of endoplasmic reticulum stress response following trauma-hemorrhage.

机译:内出血后内质网应激反应的激活。

获取原文
获取原文并翻译 | 示例
获取外文期刊封面目录资料

摘要

Hemorrhagic trauma leads to organ dysfunction, sepsis and death. There is abnormal production of proinflammatory cytokines by Kupffer cells, tissue hypoxia and liver injury following trauma-hemorrhage. The physiological conditions consequent to trauma-hemorrhage are consistent with factors necessary to initiate endoplasmic reticulum (ER) stress and unfolded protein response. However, the contribution of ER stress to apoptosis and liver injury after trauma-hemorrhage is not known. In the present study ER stress was investigated in mice that underwent trauma-hemorrhage or sham operation. Expressions of endoplasmic reticulum stress proteins Bip, ATF6, PERK, IRE1alpha, and PDI were significantly elevated in the liver after trauma-hemorrhage compared to the controls. The ER stress associated proapoptotic transcription factor CHOP protein expression was also significantly elevated in trauma-hemorrhage group. Consistent with this, enhanced DNA fragmentation was observed, confirming apoptosis, in the liver following trauma-hemorrhage. These results demonstrate the initiation of ER stress and its role in apoptosis and liver injury, subsequent to hemorrhagic trauma.
机译:出血性创伤导致器官功能障碍,败血症和死亡。创伤性出血后,库普弗细胞,组织缺氧和肝损伤导致促炎细胞因子异常产生。外伤性出血导致的生理状况与引发内质网(ER)应激和未反应的蛋白质反应所必需的因素一致。但是,ER应激对创伤性出血后细胞凋亡和肝损伤的贡献尚不清楚。在本研究中,对遭受创伤,出血或假手术的小鼠的ER应激进行了研究。与对照组相比,创伤性出血后肝脏内质网应激蛋白Bip,ATF6,PERK,IRE1alpha和PDI的表达明显升高。在外伤出血组中,与内质网应激相关的促凋亡转录因子CHOP蛋白表达也显着升高。与此相一致,创伤出血后在肝脏中观察到增强的DNA片段化,证实了细胞凋亡。这些结果证明了出血性创伤后内质网应激的启动及其在细胞凋亡和肝损伤中的作用。

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