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Glucocorticoid-Mediated Repression of Nuclear factor-κ B-dependent Transcription Involves Direct Interference with Transactivation
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Glucocorticoid-Mediated Repression of Nuclear factor-κ B-dependent Transcription Involves Direct Interference with Transactivation
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Journal Article
Glucocorticoid-Mediated Repression of Nuclear factor-κ B-dependent Transcription Involves Direct Interference with Transactivation
1997
Overview
Glucocorticoids exert multiple anti-inflammatory activities, one of which is the inhibition of transcription dependent on the nuclear factor (NF)-κ B. It has been suggested that the effect of dexamethasone (DEX), a glucocorticoid analog, is attributed to an increased production of the inhibitory Iκ B molecule, which in turn would bind and remove activated, DNA-bound NF-κ B complexes in the cell nucleus. Upon investigating DEX-mediated repression of interleukin-6 expression induced by tumor necrosis factor, DEX treatment was found to act directly on NF-κ B-dependent transcription, without changing the expression level of Iκ B. Neither the mRNA of Iκ B nor the protein was significantly elevated by a combined treatment with tumor necrosis factor and DEX of murine endothelial or fibroblast cells. The DNA-binding activity of induced NF-κ B also remained unchanged after stimulation of cells with DEX. Evidence for a direct nuclear mechanism of action was obtained by analysis of cell lines stably expressing a fusion protein between the DNA-binding domain of the yeast Ga14 protein and the transactivating p65 subunit of NF-κ B. Expression of a Ga14-dependent luciferase reporter gene activated by this nuclear fusion protein was also strongly repressed after addition of DEX. Because the DNA-binding activity of the Ga14 fusion protein was not affected by DEX, it can be concluded that the reduction of gene activation was caused by interference of the activated glucocorticoid receptor with the transactivation potential of the NF-κ B p65 subunit.
Publisher
National Academy of Sciences of the United States of America
Subject
