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Updated: May 5, 2026
An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
Estrogen modulates cardiac growth through an estrogen receptor α-dependent mechanism in healthy ovariectomized mice
Georgios Kararigas1, Ba Tiep Nguyen2, Hubertus Jarry3
1Institute of Gender in Medicine and Center for Cardiovascular Research, Charite University Hospital, Berlin, Germany.
Abstract:
The modulation of cardiac growth by estrogen in healthy mice is not completely understood. The aim was to investigate the effects of estrogen on cardiac growth in healthy mice lacking either estrogen receptor (ER) α or β. Wild-type (WT), ERα knockout (ERKO) and ERβ knockout (BERKO) 2-month-old mice were ovariectomized and randomly assigned to groups receiving an estradiol (E2)-containing or soy-free (control, CON) diet (n=5-7/group). After three months of E2 administration, WT and BERKO mice had significantly lower body weight, higher relative uterus and heart weight than CON mice, while there was no major E2 effect in ERKO mice. Furthermore, there was a higher concentration of E2-responsive genes Igf1 and Myocd in WT and BERKO but not in ERKO mice. Together, these findings indicate that the estrogenic regulation of cardiac growth in healthy mice is primarily mediated through ERα and not ERβ.
Insights
Estrogen influences cardiac growth in mice primarily via estrogen receptor-alpha (ERα), not estrogen receptor-beta (ERβ). This finding clarifies the specific role of ERα in regulating heart development and function.
Area of Science:
- Cardiovascular Biology
- Endocrinology
- Molecular Genetics
Background:
- Estrogen's role in cardiac growth is not fully understood.
- Estrogen receptors (ERα and ERβ) mediate estrogenic effects.
- Investigating specific receptor roles is crucial for understanding cardiac physiology.
Purpose of the Study:
- To determine the specific roles of ERα and ERβ in estrogen-mediated cardiac growth.
- To elucidate the molecular mechanisms underlying estrogen's effects on the heart.
- To compare cardiac responses to estrogen in wild-type and knockout mouse models.
Main Methods:
- Utilized wild-type (WT), ERα knockout (ERKO), and ERβ knockout (BERKO) mice.
- Ovariectomy followed by administration of estradiol (E2) or control diet.
- Measured body weight, relative organ weights (uterus, heart), and gene expression (Igf1, Myocd).
Main Results:
- WT and BERKO mice showed decreased body weight and increased relative heart/uterus weight with E2 treatment.
- ERKO mice exhibited no significant changes in body or organ weights.
- E2-responsive gene expression (Igf1, Myocd) was elevated in WT and BERKO but not ERKO mice.
Conclusions:
- Estrogenic regulation of cardiac growth in healthy mice is predominantly mediated by ERα.
- ERβ does not play a significant role in this process.
- Findings highlight ERα as the key mediator of estrogen's impact on cardiac development.
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