© 2000 American Heart Association, Inc.
Molecular Medicine |
Competition for p300 Regulates Transcription by Estrogen Receptors and Nuclear Factor-
B in Human Coronary Smooth Muscle Cells
From the Cardiology Branch (E.S., R.O.C.) and Pathology Section (Z-X.Y., K.T., V.J.F.), National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Correspondence to Edith Speir, National Institutes of Health, Building 10, Room 7B15, 10 Center Dr, Bethesda, MD 20892-1650. E-mail speire{at}nih.gov
Abstract—Previous
studies suggest that estrogen may prevent expression of cell adhesion
molecules implicated in vascular inflammation associated with
atherosclerosis. We demonstrate the interaction and reciprocal
interference of estrogen receptors (ERs) with p65, the nuclear
factor-
B component, in smooth muscle cells that express ER
and
ERß after exposure to 17ß-estradiol for 48 to 72 hours. ER and p65
do not associate directly, as shown by lack of coprecipitation, but
instead compete for limiting amounts of p300, a close relative of the
CREB-binding protein. Overexpressed p300 significantly reduced the
inhibitory effect of ER on p65-dependent transcription as well as the
inhibitory effect of p65 on ER-dependent transcription. These actions
were ligand-dependent. The expression of both ER and nuclear
factor-B–dependent reporter genes was partially rescued from ER/p65
mutual inhibition by transient transfection of smooth muscle cells with
a p300 expression vector. These actions of 17ß-estradiol may play an
important role in the cytokine-induced expression of immune and
inflammatory genes implicated in
atherogenesis.
Key Words: estrogen receptors /ß • intercellular adhesion molecule-1 • nuclear factor-B • transcriptional coactivator p300 • vascular smooth muscle cells
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