Source:http://linkedlifedata.com/resource/pubmed/id/21435447
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2011-3-25
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pubmed:abstractText |
Emerging evidence suggests that proinflammatory cytokines, including tumor necrosis factor-? (TNF-?) and interleukin-6 (IL-6), play a critical role in the initiation and progression of liver regeneration; however, relatively little is known about the role of anti-inflammatory cytokine IL-10 in liver regeneration after partial hepatectomy (PHx). Here, we examined the role of IL-10 in liver regeneration using a model of PHx in several strains of genetically modified mice. After PHx, expression of IL-10 mRNA in the liver and spleen was significantly elevated. Such elevation was diminished in TLR4 mutant mice. Compared with wild-type mice, IL-10(-/-) mice had higher levels of expression of proinflammatory cytokines (IL-6, TNF-?, and IFN-?) and inflammatory markers (CCR2 and F4/80) in the liver, as well as higher serum levels of proinflammatory cytokines after PHx. The number of neutrophils and macrophages was also higher in the livers of IL-10(-/-) mice than in wild-type mice after PHx. Liver regeneration as determined by BrdU incorporation after PHx was higher in IL-10(-/-) mice than in wild-type mice, which was associated with higher levels of activation of IL-6 downstream signal STAT3 in the liver. An additional deletion of STAT3 in hepatocytes significantly reduced liver regeneration in IL-10(-/-) mice after PHx. Collectively, IL-10 plays an important role in negatively regulating liver regeneration via limiting inflammatory response and subsequently tempering hepatic STAT3 activation.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1525-2191
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pubmed:author | |
pubmed:copyrightInfo |
Copyright © 2011 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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pubmed:issnType |
Electronic
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pubmed:volume |
178
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1614-21
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pubmed:meshHeading |
pubmed-meshheading:21435447-Animals,
pubmed-meshheading:21435447-Cytokines,
pubmed-meshheading:21435447-Gene Expression Regulation,
pubmed-meshheading:21435447-Hepatectomy,
pubmed-meshheading:21435447-Hepatocytes,
pubmed-meshheading:21435447-Inflammation,
pubmed-meshheading:21435447-Interleukin-10,
pubmed-meshheading:21435447-Liver,
pubmed-meshheading:21435447-Liver Regeneration,
pubmed-meshheading:21435447-Male,
pubmed-meshheading:21435447-Mice,
pubmed-meshheading:21435447-Mice, Knockout,
pubmed-meshheading:21435447-Mice, Transgenic,
pubmed-meshheading:21435447-STAT3 Transcription Factor,
pubmed-meshheading:21435447-Spleen
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pubmed:year |
2011
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pubmed:articleTitle |
Enhanced liver regeneration in IL-10-deficient mice after partial hepatectomy via stimulating inflammatory response and activating hepatocyte STAT3.
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pubmed:affiliation |
Institute of Clinical Pharmacology, Ministry of Education, Anhui Medical University, Anhui, China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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