Increased expression of estrogen receptor-β mRNA in male blood vessels after vascular injury

Volkhard Lindner, Sung K. Kim, Richard H. Karas, George G.J.M. Kuiper, Jan Åke Gustafsson, Michael E. Mendelsohn

Research output: Contribution to journalArticle

270 Scopus citations

Abstract

Estrogen exerts direct effects on vascular endothelial and smooth muscle cells that are important for vascular protection. Estrogen receptor-α (ERα) 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 ERα knockout mice. These mice express the newly described estrogen receptor- β (ERβ) in their aortas, suggesting that ERβ may also mediate some of the direct effects of estrogen on the vasculature. In this study, the level of expression of ERα and ERβ mRNA in male rat aortas was examined before and after vascular injury using en face (Hautchen) preparations and in situ hybridization. Little or no change in ERα expression was observed after vascular injury in either vascular endothelial or smooth muscle cells at any time point. In contrast, ERβ mRNA was found to be expressed markedly after balloon injury. In endothelial cells, ERβ was increased by 2 days after injury, and high levels of expression were maintained at 8 and 14 days. Furthermore, ERβ 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 ERβ in male vascular tissues and the induction of ERβ mRNA expression after vascular injury, supporting a role for ERβ in the direct vascular effects of estrogen.

Original languageEnglish (US)
Pages (from-to)224-229
Number of pages6
JournalCirculation Research
Volume83
Issue number2
DOIs
StatePublished - Jul 27 1998

Keywords

  • Endothelium
  • Estrogen receptor
  • Knockout mouse
  • Vascular injury
  • Vasculature

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

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