Activation of endoplasmic reticulum stress response following trauma-hemorrhage

Bixi Jian, Chi Hsun Hsieh, Jianguo Chen, Mashkoor Choudhry, Kirby Bland, Irshad Chaudry, Raghavan Raju

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)621-626
Number of pages6
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Issue number11
StatePublished - Nov 2008
Externally publishedYes


  • Apoptosis
  • ER stress
  • Hemorrhage
  • Hypoxia
  • Shock
  • Trauma

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology


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