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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2009-1-2
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pubmed:abstractText |
Period 2 (Per2) is a key component of the core clock oscillator and is involved in regulating a number of different biological processes and pathways. Here we report that Per2 plays a protective role in carbon tetrachloride (CCl(4))-induced hepatotoxicity via the modulation of uncoupling protein-2 (Ucp2) gene expression in mice. Hepatic injury after acute CCl(4) injection was monitored in both wild-type and Per2-null mice. At the 12-hour time point after CCl(4) treatment, many more vacuolations were observed in the liver tissues of Per2-null mice whereas fatty tissue degeneration primarily occurred in the liver tissues of wide-type mice. Serum alanine and aspartate aminotransferase activities were elevated in Per2-null mice compared with wide-type mice at 24 hours after CCl(4) treatment, which was in agreement with the observation of significantly larger areas of centrilobular necrosis in the livers of Per2-null mice. A deficit of the Per2 gene enhanced Ucp2 gene expression levels in the liver. As a consequence, intracellular levels of ATP markedly decreased in the liver, allowing increased production of toxic CCl(4) derivatives. The absence of Per2 expression caused a dramatic elevation of Clock expression and influenced Ucp2 through a mechanism that involved a Clock-controlled PPAR-alpha signal transduction pathway. Our studies suggest that the Per2 gene functions in hepatocyte protection from chemical toxicants via the regulation of hepatic Ucp2 gene expression levels.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-10026188,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-10400310,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-10841206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-10841207,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-11376163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-11475423,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-11752126,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-11782473,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-12015981,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-15500444,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/19056852-9875305
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CLOCK Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Tetrachloride,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Cycle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Clock protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Ion Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Mitochondrial Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/PPAR alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Per2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Period Circadian Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/mitochondrial uncoupling protein 2
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1525-2191
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
174
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
63-70
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:19056852-Animals,
pubmed-meshheading:19056852-CLOCK Proteins,
pubmed-meshheading:19056852-Carbon Tetrachloride,
pubmed-meshheading:19056852-Cell Cycle Proteins,
pubmed-meshheading:19056852-Gene Expression,
pubmed-meshheading:19056852-Ion Channels,
pubmed-meshheading:19056852-Liver,
pubmed-meshheading:19056852-Mice,
pubmed-meshheading:19056852-Mice, Mutant Strains,
pubmed-meshheading:19056852-Mitochondrial Proteins,
pubmed-meshheading:19056852-Nuclear Proteins,
pubmed-meshheading:19056852-PPAR alpha,
pubmed-meshheading:19056852-Period Circadian Proteins,
pubmed-meshheading:19056852-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19056852-Signal Transduction,
pubmed-meshheading:19056852-Trans-Activators,
pubmed-meshheading:19056852-Transcription Factors
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pubmed:year |
2009
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pubmed:articleTitle |
The protective role of Per2 against carbon tetrachloride-induced hepatotoxicity.
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pubmed:affiliation |
Center for Molecular Metabolism, Nanjing University of Science and Technology, Nanjing, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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