Source:http://linkedlifedata.com/resource/pubmed/id/14646597
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007589,
umls-concept:C0017262,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0079904,
umls-concept:C0166417,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0392756,
umls-concept:C1257743,
umls-concept:C1314939,
umls-concept:C1456820,
umls-concept:C1511938,
umls-concept:C2911684
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pubmed:issue |
5
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pubmed:dateCreated |
2003-12-3
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pubmed:abstractText |
TNF-alpha, a trimeric cytokine, was known to inhibit differention of preadipocytes to adipocytes. In the present study, we investigated signal mediators working downstream of TNF-alpha using murine 3T3-L1 cells. TNF-alpha induced activation of both c-jun NH(2)-terminal kinase (JNK) and nuclear transcription factor-kappaB (NF-kappaB) in 3T3-L1 cells. Blockage of these two mediators activities by specific inhibitors, SP600125 and Ad-IkappaBalpha-SR restored adipogenesis differentiation suggesting their involvement in the inhibited differentiation of 3T3-L1 cells by TNF-alpha. Consistent with previous studies, peroxisome proliferator-activated receptor gamma (PPARgamma) a key transcriptional regulator was remarkably reduced by TNF-alpha treatment. Compared with adipogenesis, however, SP600125, a chemical JNK inhibitor hardly relieved TNF-alpha effect on PPARgamma expression whereas S32A/S36A mutant of IkappaBalpha considerably recovered PPARgamma expression, indicating that two signal mediators exploit separable main routes to achieve reduced adipogenesis. These results suggest that inhibition of 3T3-L1 cells differentiation by TNF-alpha is partly implemented through NF-kappaB and one of its downstream effectors be PPARgamma.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cytoplasmic and Nuclear,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1226-3613
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
31
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pubmed:volume |
35
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
431-7
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:14646597-3T3-L1 Cells,
pubmed-meshheading:14646597-Adipocytes,
pubmed-meshheading:14646597-Animals,
pubmed-meshheading:14646597-Cell Differentiation,
pubmed-meshheading:14646597-Gene Expression Regulation,
pubmed-meshheading:14646597-Mice,
pubmed-meshheading:14646597-NF-kappa B,
pubmed-meshheading:14646597-Promoter Regions, Genetic,
pubmed-meshheading:14646597-RNA, Messenger,
pubmed-meshheading:14646597-Receptors, Cytoplasmic and Nuclear,
pubmed-meshheading:14646597-Transcription Factors,
pubmed-meshheading:14646597-Tumor Necrosis Factor-alpha
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pubmed:year |
2003
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pubmed:articleTitle |
NF-kappaB is involved in the TNF-alpha induced inhibition of the differentiation of 3T3-L1 cells by reducing PPARgamma expression.
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pubmed:affiliation |
Department of Biochemistry, College of Medicine, Dankook University, San 29 Anseo-dong, Cheonan 330-714, Korea.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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