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B Activity by Glucocorticoids
Hubrecht Laboratory Netherlands Institute for Developmental Biology 3584 CT Utrecht, The Netherlands
Repression of nuclear factor (NF)-
B-dependent
gene expression is one of the key characteristics by which
glucocorticoids exert their antiinflammatory and immunosuppressive
effects. In vitro studies have shown protein-protein
interactions between NF-B and the glucocorticoid receptor, possibly
explaining their mutual repression of transcriptional activity.
Furthermore, glucocorticoid-induced transcription of IB
was
presented as a mechanism in mediation of immunosuppression by
glucocorticoids. At present, the relative contribution of each
mechanism has not been investigated. We show that dexamethasone induced
IB gene transcription in human pulmonary epithelial A549 cells.
However, this enhanced IB synthesis did not cause repression of
NF-B DNA-binding activity. In addition, dexamethasone was still
able to inhibit the expression of NF-B target genes
(cyclooxygenase-2, intercellular adhesion molecule-1) in the absence of
protein synthesis. Furthermore, we show that the antihormone RU486 did
not induce IB expression. However, RU486 was still able to
induce, albeit less efficiently, both glucocorticoid- and progesterone
receptor-mediated repression of endogenous NF-B target gene
expression in A549 cells and the breast cancer cell line T47D,
respectively. Taken together, these results indicate that induced
IB expression accounts for only part of the repression of NF-B
activity by glucocorticoids and progestins. In addition,
protein-protein interactions between NF-B and the glucocorticoid or
progesterone receptor, resulting in repression of NF-B activity,
seem also to be involved. We therefore conclude that NF-B activity
is repressed via a dual mechanism involving both protein-protein
interactions and induction of IB.
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