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Am J Physiol Heart Circ Physiol (September 16, 2004). doi:10.1152/ajpheart.00723.2004
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Submitted on July 20, 2004
Accepted on September 13, 2004

The Beta Estrogen Receptor Mediates Male-Female Differences in the Development of Pressure Overload Hypertrophy

Maryanne Skavdahl1, Charles Steenbergen2, James Clark3, Page Myers3, Tracy Demianenko3, Lan Mao4, Howard A. Rockman4, Kenneth S. Korach5, and Elizabeth Murphy6*

1 Laboratory of Signal Transduction, NIEHS, NIH, Research Triangle Park, NC, USA; Department of Pathology, Duke University Medical Center, Durham, NC, USA
2 Department of Pathology, Duke University Medical Center, Durham, NC, USA
3 Comparative Medicine Brance, NIEHS, NIH, Research Triangle Park, NC, USA
4 Department of Medicine, Duke University, Durham, NC, USA
5 Laboratory of Reporductive and Developmental Toxicology, NIEHS, NIH, Research Triangle Park, NC, USA
6 Laboratory of Signal Transduction, NIEHS, NIH, Research Triangle Park, NC, USA

* To whom correspondence should be addressed. E-mail: murphy1{at}niehs.nih.gov.

The goal of this study was to determine the role of estrogen receptor subtypes in the development of pressure overload hypertrophy in mice. Epidemiological studies have suggested gender differences in the development of hypertrophy and heart disease, but the mechanism and the role of estrogen receptor subtypes is not established. We performed transverse aortic constriction (TAC) and sham operations in male and female wild type (WT) mice and mice lacking functional alpha estrogen receptor ({alpha}-ERKO) and mice lacking beta estrogen receptor ({beta}-ERKO). Body, heart, and lung weights were measured 2 weeks post surgery. WT male mice subjected to TAC showed a 64% increase in heart to body weight (HW/BW) ratio compared to sham, and WT males have increased lung weight at 2 weeks. WT female mice subjected to TAC showed a 31% increase in HW/BW compared to sham, which was significantly less than their male counterparts and no evidence of heart failure. {alpha}-ERKO females developed a HW/BW ratio nearly identical to that seen in WT littermate females in response to TAC, indicating that the alpha estrogen receptor is not essential for the attenuation of hypertrophy observed in WT females. In contrast, {beta}-ERKO females responded to TAC with a significantly greater increase in HW/BW ratio than WT littermate females. {beta}-ERKO females have lower expression of lipoprotein lipase at baselline than WT or {alpha}-ERKO females. These data suggest an important role for the {beta}-estrogen receptor in attenuating the hypertrophic response to pressure overload in females.




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