NF-κB is involved in the TNF-α induced inhibition of the differentiation of 3T3-L1 cells by reducing PPARγ expression View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2003-10

AUTHORS

Gi-Nam Chae, Sahng-June Kwak

ABSTRACT

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. More... »

PAGES

431

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/emm.2003.56

DOI

http://dx.doi.org/10.1038/emm.2003.56

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001944732

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14646597


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