on April 20, 2006
Published online before print April 20, 2006, doi: 10.1161/01.ATV.0000223344.11128.23
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Submitted on June 15, 2005
Accepted on April 11, 2006
Estrogen Receptor 
Protects the Murine Heart Against Left Ventricular Hypertrophy
Fawzi A. Babiker ;
From the Department of Cardiology (F.A.B., D.L., E.D.), Cardiovascular Research Institute Maastricht, University Hospital Maastricht, the Netherlands; Physiologisches Institut II (R.M.), Bonn Germany; Department of Pharmacology (P.Z.), Organon NV, the Netherlands; Department of Pharmacology (B.J.), Cardiovascular Research Institute Maastricht, Maastricht University, the Netherlands; Department of Molecular Genetics (G.v.E.), Cardiovascular Research Institute Maastricht, Maastricht University, the Netherlands; Medizinische Universitätspoliklinik (C.G.), Bonn, Germany; Interuniversity Cardiology Institute of the Netherlands (P.A.D.) and Department of Cardiology (P.A.D.), Heart Lung Center Utrecht, the Netherlands.
* To whom correspondence should be addressed. E-mail: c.grohe{at}uni-bonn.de.
Background--Left ventricular hypertrophy (LVH) displays significant gender-based differences. 17
-estradiol (E2) plays an important role in this process because it can attenuate pressure overload hypertrophy via 2 distinct estrogen receptors (ERs): ER
and ER. However, which ER is critically involved in the modulation of LVH is poorly understood. We therefore used ER-deficient (ER-/-) and ER-deficient (ER-/-) mice to analyze the respective ER-mediated effects.
Methods and Results--Respective ER-deficient female mice were ovariectomized and were given E2 or placebo subcutaneously using 60-day release pellets. After 2 weeks, they underwent transverse aortic constriction (TAC) or sham operation. In ER-/- animals, TAC led to a significant increase in ventricular mass compared with sham operation. E2 treatment reduced TAC induced cardiac hypertrophy significantly in wild-type (WT) and ER-/- mice but not in ER-/- mice. Biochemical analysis showed that E2 blocked the increased phosphorylation of p38-mitogen-activated protein kinase observed in TAC-treated ER-/- mice. Moreover, E2 led to an increase of ventricular atrial natriuretic factor expression in WT and ER-/- mice.
Conclusions--These findings demonstrate that E2, through ER-mediated mechanisms, protects the murine heart against LVH.
Key words: hypertrophy • hormones • myocardium • gender
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