Original Contributions |
From the Molecular Cardiology and Tupper Research Institutes (S.K.K., R.H.K., M.E.M.) and the Surgical Research Division (S.K.K.), New England Medical Center, Tufts University School of Medicine, Boston, Mass; the Maine Medical Center (V.L.), Portland, Me; and the Department of Medical Nutrition and Center for Biotechnology (G.G.J.M.K., J.-Å.G.), Karolinska Institute, Uppsala, Sweden.
Correspondence to Michael E. Mendelsohn, MD, Molecular Cardiology Research Center, 750 Washington St, #80, Boston, MA 02111. E-mail michael.mendelsohn{at}es.nemc.org
AbstractEstrogen exerts direct
effects on vascular endothelial and smooth muscle cells
that are important for vascular protection. Estrogen receptor-
(ER
) is expressed in vascular cells from males and females and may
mediate some of the effects of estrogen on vascular tissue. However, we
recently found that estrogen is able to protect against vascular injury
in ovariectomized female ER
knockout mice. These mice express the
newly described estrogen receptor-ß (ERß) in their aortas,
suggesting that ERß may also mediate some of the direct effects of
estrogen on the vasculature. In this study, the level of expression of
ER
and ERß mRNA in male rat aortas was examined before and after
vascular injury using en face (Häutchen) preparations and in situ
hybridization. Little or no change in ER
expression was observed
after vascular injury in either vascular endothelial or
smooth muscle cells at any time point. In contrast, ERß mRNA was
found to be expressed markedly after balloon injury. In
endothelial cells, ERß was increased by 2 days after
injury, and high levels of expression were maintained at 8 and 14 days.
Furthermore, ERß expression was high in luminal smooth muscle cells
at 8 and 14 days after injury and had decreased to low levels by 28
days after injury. These data demonstrate the presence of ERß in male
vascular tissues and the induction of ERß mRNA expression after
vascular injury, supporting a role for ERß in the direct vascular
effects of estrogen.
Key Words: estrogen receptor vasculature knockout mouse vascular injury endothelium
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