(Circulation. 2000;101:1792.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
and ß
From the Divisions of Cardiology (Y.K.H., X.-D.Y., L.D.H.) and Endocrinology (L.T., J.D.G., K.B.H.), Department of Medicine, University of Colorado Health Sciences Center, Denver, Colo.
Correspondence to Lawrence D. Horwitz, MD, Cardiology B130, University of Colorado Health Sciences Center, Denver, CO 80262. E-mail lawrence.horowitz{at}UCHSC.edu
BackgroundEstrogens have
vascular effects through the activation of estrogen receptors (ERs). In
addition to ER
, the first ER to be cloned, a second subtype called
ERß has recently been discovered.
Methods and ResultsUsing a reverse-transcriptase polymerase
chain reaction assay that employs the same primer pair to
simultaneously amplify ER
and ERß transcripts, we
found that ERß is the ER form that is predominantly expressed in
human vascular smooth muscle, particularly in women. The
transcriptional effects of the 2 ERs in transfected HeLa cells
differed. In response to 17ß-estradiol, ER
is a stronger
transactivator than ERß at low receptor concentrations.
However, at higher receptor concentrations, ER
activity
self-squelches, and ERß is a stronger transactivator.
Tamoxifen has partial agonist effects with ER
but not with
ERß.
ConclusionsThe protective effects of estrogens in the cardiovascular system of women may be due to the genomic effects of ERß in vascular tissue.
Key Words: muscle, smooth receptors, estrogen coronary disease human
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