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Claudin-5 as a novel estrogen target in vascular endothelium

Malgorzata Burek1, Paula A Arias-Loza, Norbert Roewer

  • 1Department of Anaesthesia and Critical Care, Institute of Anatomy and Cell Biology, University of Würzburg, Würzburg, Germany. Burek_M@klinik.uni-wuerzburg.de

Arteriosclerosis, Thrombosis, and Vascular Biology
|November 14, 2009
PubMed
Abstract

Insights

Estrogen directly targets claudin-5, a key junctional protein in brain and heart endothelial cells. This estrogen-induced increase in claudin-5 enhances vascular barrier function.

Area of Science:

  • Endocrinology
  • Vascular Biology
  • Molecular Biology

Background:

  • Estrogens significantly influence vascular physiology and function.
  • Identifying direct estrogen targets in vascular endothelium is crucial for understanding its roles.

Purpose of the Study:

  • To identify direct estrogen target genes within junctional proteins.
  • To investigate the role of estrogens in regulating claudin-5 expression in endothelial cells.

Main Methods:

  • Utilized murine endothelial cell lines (brain and heart) expressing estrogen receptors (ERalpha and ERbeta).
  • Treated cells with 17beta-estradiol (E2) and an ERbeta agonist (diarylpropionitrile).
  • Analyzed claudin-5 promoter activity, mRNA, and protein levels in vitro and in vivo (ovariectomized mice, ERbeta knockout mice).

Main Results:

  • 17beta-estradiol upregulated claudin-5 expression, promoter activity, mRNA, and protein levels in brain and heart endothelial cells.
  • In vivo studies confirmed increased claudin-5 in E2-treated mice and decreased levels in ERbeta knockout mice.
  • ERbeta activation mimicked E2 effects, indicating ERbeta's role in mediating claudin-5 regulation.

Conclusions:

  • Claudin-5 is identified as a novel direct estrogen target gene in vascular endothelium.
  • Estrogen administration increases claudin-5 levels in brain and heart endothelium, both in vitro and in vivo.
  • Elevated claudin-5 may enhance vascular structural integrity and barrier function.

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