CXC receptor-2 knockout genotype increases X-linked inhibitor of apoptosis protein and protects mice from acetaminophen hepatotoxicity.
CXC receptor-2 knockout genotype increases X-linked inhibitor of apoptosis protein and protects mice from acetaminophen hepatotoxicity.
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DOI：
10.1002/hep.23715
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发表时间：
2010-08
期刊：
影响因子：
13.5
通讯作者：
Colletti, Lisa M.
中科院分区：
文献类型：
--
作者：
Hu, Bin;Colletti, Lisa M.
Although it is a commonly used analgesic, acetaminophen can be highly hepatotoxic. This study seeks to further investigate the mechanisms involved in acetaminophen-induced hepatotoxicity, as well as the role of CXCR2 receptor/ligand interactions in the liver’s response to and recovery from acetaminophen toxicity. The CXC chemokines and their receptor, CXCR2, are important inflammatory mediators, as well as being involved in the control of some types of cellular proliferation. CXCR2 knock out mice exposed to an LD50 dose of acetaminophen have a significantly lower mortality rate as compared to wild type mice. This difference is at least partially attributable to a significantly decreased rate of apoptosis in the CXCR2 knock out mice versus wild type; there were no differences seen in hepatocyte proliferation in wild types versus knock outs after this injury. The decreased rate of apoptosis in the knock out mice correlated with an almost undetectable and significantly decreased level of activated caspace-3, and significantly increased levels of X-linked inhibitor of apoptosis protein (XIAP), which also correlated with increased levels of NF-KB p52 and decreased levels of JNK, providing a possible mechanism for the decrease in apoptosis seen in the CXCR2 knock out mice.
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影响因子：
20.1
作者：
Levkau, B;Garton, KJ;Breithardt, G
通讯作者：
Breithardt, G
影响因子：
4.3
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Bubici, C;Papa, S;Franzoso, G
通讯作者：
Franzoso, G
影响因子：
6
作者：
Ren, XD;Carpenter, A;Colletti, L
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Colletti, L
影响因子：
4.6
作者：
Shakil, AO;Kramer, D;Rakela, J
通讯作者：
Rakela, J
影响因子：
13.5
作者：
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通讯作者：
Lentsch, Alex B.