Activation of endoplasmic reticulum stress response following trauma-hemorrhage

Academic Article

Abstract

  • 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, IRE1α, 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. © 2008 Elsevier B.V. All rights reserved.
  • Published In

    Digital Object Identifier (doi)

    Pubmed Id

  • 9003025
  • Author List

  • Jian B; Hsieh CH; Chen J; Choudhry M; Bland K; Chaudry I; Raju R
  • Start Page

  • 621
  • End Page

  • 626
  • Volume

  • 1782
  • Issue

  • 11