Semin Reprod Med 2012; 30(01): 46-61
DOI: 10.1055/s-0031-1299597
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Estrogen Receptor-α and Estrogen Receptor-β in the Uterine Vascular Endothelium during Pregnancy: Functional Implications for Regulating Uterine Blood Flow

Mayra B. Pastore
1   Departments of Obstetrics/Gynecology, Perinatal Research Laboratories
*   Both authors have contributed equally to this manuscript.
,
Sheikh O. Jobe
1   Departments of Obstetrics/Gynecology, Perinatal Research Laboratories
*   Both authors have contributed equally to this manuscript.
,
Jayanth Ramadoss
1   Departments of Obstetrics/Gynecology, Perinatal Research Laboratories
,
Ronald R. Magness
1   Departments of Obstetrics/Gynecology, Perinatal Research Laboratories
2   Pediatrics
3   Animal Sciences, University of Wisconsin-Madison, Madison, Wisconsin
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Publikationsverlauf

Publikationsdatum:
23. Januar 2012 (online)

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Abstract

The steroid hormone estrogen and its classical estrogen receptors (ERs), ER-α and ER-β, have been shown to be partly responsible for the short- and long-term uterine endothelial adaptations during pregnancy. The ER-subtype molecular and structural differences coupled with the differential effects of estrogen in target cells and tissues suggest a substantial functional heterogeneity of the ERs in estrogen signaling. In this review we discuss (1) the role of estrogen and ERs in cardiovascular adaptations during pregnancy, (2) in vivo and in vitro expression of ERs in uterine artery endothelium during the ovarian cycle and pregnancy, contrasting reproductive and nonreproductive arterial endothelia, (3) the structural basis for functional diversity of the ERs and estrogen subtype selectivity, (4) the role of estrogen and ERs on genomic responses of uterine artery endothelial cells, and (5) the role of estrogen and ERs on nongenomic responses in uterine artery endothelia. These topics integrate current knowledge of this very rapidly expanding scientific field with diverse interpretations and hypotheses regarding the estrogenic effects that are mediated by either or both ERs and their relationship with vasodilatory and angiogenic vascular adaptations required for modulating the dramatic physiological rises in uteroplacental perfusion observed during normal pregnancy.