Activation of endoplasmic reticulum stress response following trauma-hemorrhage

作者：Jian Bixi; Hsieh Chi Hsun; Chen Jianguo; Choudhry Mashkoor; Bland Kirby; Chaudry Irshad; Raju Raghavan^*

来源：Biochimica et Biophysica Acta-Molecular Basis of Disease, 2008, 1782(11): 621-626.

DOI：10.1016/j.bbadis.2008.08.007

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

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, IRE1 alpha, 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.

• 出版日期2008-11