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Original Articles

Estrogen Receptor-β Signals Left Ventricular Hypertrophy Sex Differences in Normotensive Deoxycorticosterone Acetate-Salt Mice

Dennis Gürgen, Björn Hegner, Angelika Kusch, Rusan Catar, Lyubov Chaykovska, Uwe Hoff, Volkmar Gross, Torsten Slowinski, Andrey C. da Costa Goncalves, Ulrich Kintscher, Jan-Åke Gustafsson, Friedrich C. Luft, Duska Dragun
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https://doi.org/10.1161/HYPERTENSIONAHA.110.166157
Hypertension. 2011;HYPERTENSIONAHA.110.166157
Originally published February 7, 2011
Dennis Gürgen
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Björn Hegner
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Angelika Kusch
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Rusan Catar
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Lyubov Chaykovska
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Uwe Hoff
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Volkmar Gross
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Torsten Slowinski
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Andrey C. da Costa Goncalves
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Ulrich Kintscher
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Jan-Åke Gustafsson
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Friedrich C. Luft
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Duska Dragun
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Abstract

We found earlier that deoxycorticosterone acetate-salt treatment causes blood pressure–independent left ventricular hypertrophy, but only in male mice. To test the hypothesis that the estrogen receptor-β (ERβ) protects the females from left ventricular hypertrophy, we treated male and female ERβ-deficient (ERβ−/−) mice and their male and female littermates (wild-type [WT]) with deoxycorticosterone acetate-salt and made them telemetrically normotensive with hydralazine. WT males had increased (+16%) heart weight/tibia length ratios compared with WT females (+7%) at 6 weeks. In ERβ−/− mice, this situation was reversed. Female WT mice had the greatest heart weight/tibia length ratio increases of all of the groups (+23%), even greater than ERβ−/− males (+10%). Echocardiography revealed concentric left ventricular hypertrophy in male WT mice, whereas ERβ−/− females developed dilative left ventricular hypertrophy. The hypertrophic response in female ERβ−/− mice was accompanied by the highest degree of collagen deposition, indicating maladaptive remodeling. ERβ+/+ females showed robust protective p38 and extracellular signal–regulated kinase 1/2 signaling relationships compared with other groups. Calcineurin Aβ expression and its positive regulator myocyte-enriched calcineurin-interacting protein 1 were increased in deoxycorticosterone acetate-salt female ERβ−/− mice, yet lower than in WT males. Endothelin increased murine cardiomyocyte hypertrophy in vitro, which could be blocked by estradiol and an ERβ agonist. We conclude that a functional ERβ is essential for inducing adaptive p38 and extracellular signal–regulated kinase signaling, while reducing maladaptive calcineurin signaling in normotensive deoxycorticosterone acetate female mice. Our findings address the possibility of sex-specific cardiovascular therapies.

  • estrogen receptor-β, heart
  • hypertrophy
  • fibrosis
  • calcineurin
  • p38 MAPK
  • ERK1/2
  • Received November 1, 2010.
  • Revision received December 1, 2010.
  • Accepted January 12, 2011.
  • © 2011 American Heart Association, Inc.
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    Estrogen Receptor-β Signals Left Ventricular Hypertrophy Sex Differences in Normotensive Deoxycorticosterone Acetate-Salt Mice
    Dennis Gürgen, Björn Hegner, Angelika Kusch, Rusan Catar, Lyubov Chaykovska, Uwe Hoff, Volkmar Gross, Torsten Slowinski, Andrey C. da Costa Goncalves, Ulrich Kintscher, Jan-Åke Gustafsson, Friedrich C. Luft and Duska Dragun
    Hypertension. 2011;HYPERTENSIONAHA.110.166157, originally published February 7, 2011
    https://doi.org/10.1161/HYPERTENSIONAHA.110.166157

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    Estrogen Receptor-β Signals Left Ventricular Hypertrophy Sex Differences in Normotensive Deoxycorticosterone Acetate-Salt Mice
    Dennis Gürgen, Björn Hegner, Angelika Kusch, Rusan Catar, Lyubov Chaykovska, Uwe Hoff, Volkmar Gross, Torsten Slowinski, Andrey C. da Costa Goncalves, Ulrich Kintscher, Jan-Åke Gustafsson, Friedrich C. Luft and Duska Dragun
    Hypertension. 2011;HYPERTENSIONAHA.110.166157, originally published February 7, 2011
    https://doi.org/10.1161/HYPERTENSIONAHA.110.166157
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