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J. Biol. Chem., Vol. 276, Issue 32, 30208-30215, August 10, 2001
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From the Thoracic Medicine, Imperial College School of Medicine at
the National Heart and Lung Institute, Dovehouse St.,
London SW3 6LY, United Kingdom
Glucocorticoids acting through their
specific receptor can either enhance or repress gene transcription.
Dexamethasone represses interleukin-1
p65-activated Histone Acetyltransferase Activity Is
Repressed by Glucocorticoids
MIFEPRISTONE FAILS TO RECRUIT HDAC2 TO THE p65-HAT
COMPLEX*
,
-stimulated histone
acetylation and granulocyte-macrophage colony-stimulating factor
expression through a combination of direct inhibition of p65-associated
histone acetyltransferase (HAT) activity and by recruiting histone
deacetylase 2 (HDAC2) to the p65-HAT complex. Here we show that
mifepristone, a glucocorticoid receptor partial agonist, has no ability
to induce gene expression but represses interleukin-1-stimulated
histone acetylation and granulocyte-macrophage colony-stimulating
factor release by 50% maximally. Mifepristone was able to inhibit
p65-associated HAT activity to the same extent as dexamethasone but
failed to inhibit the natural promoter to an equal extent due to an
inability to recruit HDAC2 to the p65-associated HAT complex. These
data suggest that the maximal repressive actions of glucocorticoids
require recruitment of HDAC2 to a p65-HAT complex. These data also
suggest that pharmacological manipulation of specific histone
acetylation status is a potentially useful approach for the treatment
of inflammatory diseases.
*
This work was funded by the Clinical Research Committee
(Brompton Hospital), the British Lung Foundation, and GlaxoSmithKline.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
A European Respiratory Society Clinical Fellow.
§
To whom correspondence should be addressed: Thoracic Medicine,
Imperial College School of Medicine at the National Heart and Lung
Institute, Dovehouse St., London SW3 6LY, United Kingdom. Tel.: 44 171 352 8121; Fax: 44 171 351 8126; E-mail: ian.adcock@ic.ac.uk.
Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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