ISSN:
1572-9931
Keywords:
lipopolysaccharide
;
inflammation
;
nuclear factor κ-B
;
Inhibitor of NF-κB
;
dedifferentiated hepatoma
;
hepatic gene expression
;
hepatocyte nuclear factor 1α
;
hepatocyte nuclear factor 4
Source:
Springer Online Journal Archives 1860-2000
Topics:
Biology
,
Medicine
Notes:
Abstract Dedifferentiated rat hepatoma cells contain defects that result in the loss of hepatic gene expression, including the liver-enriched HNF4/HNF1α pathway. We examined induction of NF-κB, a key mediator of the inflammatory response, in hepatoma and dedifferentiated hepatoma cells. We show that exposure of dedifferentiated hepatoma cells, but not rat and human hepatoma cell lines, to proinflammatory cytokines or lipopolysaccharide resulted in rapid and sustained NF-κB induction. IκB-β levels, but not NF-κB subunit p65 or IκB-α levels, were elevated compared with those for parental hepatoma cells. Interestingly, LPS-mediated activation of NF-κB was found to be independent of degradation of IκB-α or IκB-β. Thus, these results suggest that loci responsible for maintaining hepatic gene expression also influence cellular responses to inflammatory agents.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1023/A:1019912314897
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