Activation of endoplasmic reticulum stress response following trauma-hemorrhage.

Activation of endoplasmic reticulum stress response following trauma-hemorrhage.
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DOI:
10.1016/j.bbadis.2008.08.007
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发表时间:
2008-11
影响因子:
6.2
通讯作者:
Raju, Raghavan
Raju, Raghavan
中科院分区:
生物学2区
文献类型:
--
作者:
Jian, Bixi;Hsieh, Chi-Hsun;Chen, Jianguo;Choudhry, Mashkoor;Bland, Kirby;Chaudry, Irshad;Raju, Raghavan

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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. Expression 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.
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