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 journalArticle

38 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)621-626
Number of pages6
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1782
Issue number11
DOIs
StatePublished - Nov 1 2008
Externally publishedYes

Keywords

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

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

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