The ER stress pathway involving CHOP is activated in the lungs of LPS-treated mice
The ER stress pathway involving CHOP is activated in the lungs of LPS-treated mice
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DOI：
10.1093/jb/mvi143
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发表时间：
2005-10-01
影响因子：
2.7
通讯作者：
Gotoh, T
中科院分区：
文献类型：
--
作者：
Endo, M;Oyadomari, S;Gotoh, T
CHOP是一个C/EBP家族转录因子，参与内质网（ER）应激介导的凋亡。为了确定ER应激途径是否参与LPS处理的小鼠肺损伤的发病机制，小鼠腹腔内给予脂多糖（LPS）。转录激活因子（ATF）4和X-box结合蛋白（X-BP）1、CHOP基因转录激活因子和CHOP基因的mRNA在LPS处理前后被诱导表达。LPS处理诱导的细胞凋亡在Chop基因敲除小鼠的肺中被抑制。CHOP过表达诱导肺癌细胞凋亡这些结果表明，ER应激途径，包括CHOP，被激活，并在脓毒性休克肺的发病机制中发挥作用。
CHOP is a C/EBP family transcription factor involved in endoplasmic reticulum (ER) stress-mediated apoptosis. To determine if the ER stress pathway is involved in the pathogenesis of LPS-treated mouse lung injury, mice were given lipopolysaccharide (LPS) intraperitoneally. The mRNAs for activating transcription factor (ATF) 4 and X-box binding protein (X-BP) 1, transcriptional activators of the CHOP gene, and that for CHOP were induced by or after the LPS treatment. Apoptosis induced by LPS treatment was suppressed in the lungs of Chop-knockout mice. Overexpression of CHOP induced apoptosis in a lung cancer-derived cell line. These results suggest that the ER stress pathway, involving CHOP, is activated and plays a role in the pathogenesis of septic shock lung.