Increased Expression of Estrogen Receptor-ß mRNA in Male Blood Vessels After Vascular Injury

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

Abstract—Estrogen 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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