Copyright © 2005, European Society of Cardiology
17β-estradiol increases volume, apical surface and elasticity of human endothelium mediated by Na+/H+ exchange
aDepartment of Internal Medicine D, University of Muenster, Germany
bInstitute of Physiology II, University of Muenster, Germany
cDepartment of Cellular and Molecular Physiology, Yale University, New Haven, United States
dDepartment of Dermatology, University of Muenster, Germany
* Corresponding author. Klinik und Poliklinik für Innere Medizin D, Albert-Schweitzer-Str. 33, 48149 Münster, Germany. Tel.: +49 251 8347535; fax: +49 251 8349643. Email address: hillebu{at}uni-muenster.de
Objective: 17β-estradiol is known to delay the onset of atherosclerosis in women but cellular mechanisms are still unclear. Estrogens bind to specific receptors and initiate a signaling cascade that involves the activation of plasma membrane Na+/H+ exchange. We hypothesized that estrogens interfere with ion transport across the plasma membrane and thus control endothelial structure and function. Therefore, we investigated the effects of the sex steroids 17β-estradiol, progesterone, and testosterone on volume, apical surface and elasticity in human endothelium.
Methods: The atomic force microscope was used as an imaging tool and as an elasticity sensor. We applied the antiestrogen tamoxifen, the Na+/H+ exchange blocker cariporide and the epithelial Na+channel blocker amiloride to elucidate the role of transmembrane ion transport in hormone-treated human umbilical vein endothelial cells (HUVEC).
Results: Incubation with 17β-estradiol for 72 h led to a dose-dependent increase of endothelial cell volume (41%), apical cell surface (22%), and cell elasticity (53%) as compared to non-17β-estradiol treated controls. Block of the 17β-estradiol receptor by tamoxifen and of plasma membrane Na+/H+ exchange by cariporide prevented the hormone-induced changes. Progesterone and testosterone were ineffective.
Conclusions: 17β-estradiol increases HUVEC water content and HUVEC elasticity mediated by activated estrogen receptors. The estrogen response depends on the activation of plasma membrane Na+/H+ exchange. The increase in endothelial cell elasticity could be one of the vasoprotective mechanisms postulated for 17β-estradiol.
KEYWORDS HUVEC; 17β-estradiol; Atomic force microscopy; Cariporide; Tamoxifen
Time for primary review 12 days
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