Estrogen Receptor β Protects the Murine Heart Against Left Ventricular Hypertrophy

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Abstract
Background— Left ventricular hypertrophy (LVH) displays significant gender-based differences. 17β-estradiol (E2) plays an important role in this process because it can attenuate pressure overload hypertrophy via 2 distinct estrogen receptors (ERs): ERα and ERβ. However, which ER is critically involved in the modulation of LVH is poorly understood. We therefore used ERα-deficient (ERα − / − ) and ERβ-deficient (ERβ − / − ) 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 ERα − / − 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 ERα − / − mice but not in ERβ −/− mice. Biochemical analysis showed that E2 blocked the increased phosphorylation of p38–mitogen-activated protein kinase observed in TAC-treated ERα − / − mice. Moreover, E2 led to an increase of ventricular atrial natriuretic factor expression in WT and ERα − / − mice. Conclusions— These findings demonstrate that E2, through ERβ-mediated mechanisms, protects the murine heart against LVH.

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