Abstract
TNF-α, a trimeric cytokine, was known to inhibit differention of preadipocytes to adipocytes. In the present study, we investigated signal mediators working downstream of TNF-α using murine 3T3-L1 cells. TNF-α induced activation of both c-jun NH2-terminal kinase (JNK) and nuclear transcription factor-κB (NF-κB) in 3T3-L1 cells. Blockage of these two mediators activities by specific inhibitors, SP600125 and Ad-IκBα-SR restored adipogenesis differentiation suggesting their involvement in the inhibited differentiation of 3T3-L1 cells by TNF-α. Consistent with previous studies, peroxisome proliferator-activated receptor γ (PPARγ) a key transcriptional regulator was remarkably reduced by TNF-α treatment. Compared with adipogenesis, however, SP600125, a chemical JNK inhibitor hardly relieved TNF-α effect on PPARγ expression whereas S32A/S36A mutant of IκBα considerably recovered PPARγ 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-α is partly implemented through NF-κB and one of its downstream effectors be PPARγ.
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Chae, GN., Kwak, SJ. NF-κB is involved in the TNF-α induced inhibition of the differentiation of 3T3-L1 cells by reducing PPARγ expression. Exp Mol Med 35, 431–437 (2003). https://doi.org/10.1038/emm.2003.56
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DOI: https://doi.org/10.1038/emm.2003.56
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