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Estrogen receptor alpha up-regulation and redistribution in human heart failure

Shokoufeh Mahmoodzadeh^*,1, Sarah Eder^*,1, Johannes Nordmeyer^*,1, Elisabeth Ehler, Otmar Huber^||, Peter Martus^#, Jörg Weiske^||, Reinhard Pregla, Roland Hetzer and Vera Regitz-Zagrosek^*,2

^* Center for Cardiovascular Research, Charite and Deutsches Herzzentrum Berlin; Berlin, Germany;

Klinik für Herz-, Gefäss- und Thoraxchirurgie, DHZB and Charite, Berlin, Germany;

Klinik für Herz-, Gefäss- und Thoraxchirurgie, DHZB Berlin, Germany;

The Randall Division of Cell and Molecular Biophysics and the Cardiovascular Division, King’s College London, England;

^|| Institute of Clinical Chemistry and Pathobiochemistry, Charite - Campus Benjamin Franklin, Berlin, Germany; and

^# Institute for Medical Statistics and Clinical Epidemiology, Berlin, Germany

²Correspondence: Deutsches Herzzentrum Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. E-mail: vrz{at}dhzb.de

Clinical and animal studies suggest that estrogen receptors are involved in the development of myocardial hypertrophy and heart failure. In this study, we investigated whether human myocardial estrogen receptor alpha (ER) expression, localization, and association with structural proteins was altered in end stage-failing hearts. We found a 1.8-fold increase in ER mRNA and protein in end-stage human dilated cardiomyopathy (DCM, n=41), as compared with controls (n=25). ER was visualized by confocal immunofluorescence microscopy and localized to the cytoplasm, sarcolemma, intercalated discs and nuclei of cardiomyocytes. Immunofluorescence studies demonstrated colocalization of ER with ß-catenin at the intercalated disc in control hearts and immunoprecipitation studies confirmed complex formation of both proteins. Interestingly, the ER/ß-catenin colocalization was lost at the intercalated disc in DCM hearts. Thus, the ER/ß-catenin colocalization in the intercalated disc may be of functional relevance and a loss of this association may play a role in the progression of heart failure. The increase of total ER expression may represent a compensatory process to contribute to the stability of cardiac intercalated discs.—Mahmoodzadeh, S., Eder, S., Nordmeyer, J., Ehler, E., Huber, O., Martus, P., Weiske, J., Pregla, R., Hetzer, R., Regitz-Zagrosek, V. Estrogen receptor alpha up-regulation and redistribution in human heart failure.

Key Words: estrogen receptors • dilated cardiomyopathy • intercalated disc

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