scholarly journals Redistribution of NMDA Receptors in Estrogen-Receptor-β-Containing Paraventricular Hypothalamic Neurons following Slow-Pressor Angiotensin II Hypertension in Female Mice with Accelerated Ovarian Failure

2016 ◽  
Vol 104 (3) ◽  
pp. 239-256 ◽  
Author(s):  
Jose Marques-Lopes ◽  
Ephrath Tesfaye ◽  
Sigal Israilov ◽  
Tracey A. Van Kempen ◽  
Gang Wang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Angiotensin Ii ◽  
Nmda Receptors ◽  
Ovarian Failure ◽  
Estrogen Receptor Β ◽  
Hypothalamic Neurons ◽  
Female Mice

scholarly journals Estrogen Receptor β Controls Muscle Growth and Regeneration in Young Female Mice

2020 ◽  
Vol 15 (3) ◽  
pp. 577-586 ◽  
Author(s):  
Daiki Seko ◽  
Ryo Fujita ◽  
Yuriko Kitajima ◽  
Kodai Nakamura ◽  
Yuuki Imai ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Muscle Growth ◽  
Young Female ◽  
Estrogen Receptor Β ◽  
Female Mice

scholarly journals Nuclear Activation Function 2 Estrogen Receptor α Attenuates Arterial and Renal Alterations Due to Aging and Hypertension in Female Mice

2020 ◽  
Vol 9 (5) ◽  
Author(s):  
Emmanuel Guivarc'h ◽  
Julie Favre ◽  
Anne‐Laure Guihot ◽  
Emilie Vessières ◽  
Linda Grimaud ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Estrogen Receptor ◽  
Angiotensin Ii ◽  
Systolic Blood Pressure ◽  
Vascular Reactivity ◽  
Nuclear Gene ◽  
Estrogen Receptor Α ◽  
Protective Effects ◽  
Wild Type ◽  
Female Mice

Background The cardiovascular protective effects of estrogens in premenopausal women depend mainly on estrogen receptor α (ERα). ERα activates nuclear gene transcription regulation and membrane‐initiated signaling. The latter plays a key role in estrogen‐dependent activation of endothelial NO synthase. The goal of the present work was to determine the respective roles of the 2 ERα activities in endothelial function and cardiac and kidney damage in young and old female mice with hypertension, which is a major risk factor in postmenopausal women. Methods and Results Five‐ and 18‐month‐old female mice lacking either ERα (ERα −/− ), the nuclear activating function AF2 of ERα (AF2°), or membrane‐located ERα (C451A) were treated with angiotensin II (0.5 mg/kg per day) for 1 month. Systolic blood pressure, left ventricle weight, vascular reactivity, and kidney function were then assessed. Angiotensin II increased systolic blood pressure, ventricle weight, and vascular contractility in ERα −/− and AF2° mice more than in wild‐type and C451A mice, independent of age. In both the aorta and mesenteric resistance arteries, angiotensin II and aging reduced endothelium‐dependent relaxation in all groups, but this effect was more pronounced in ERα −/− and AF2° than in the wild‐type and C451A mice. Kidney inflammation and oxidative stress, as well as blood urea and creatinine levels, were also more pronounced in old hypertensive ERα −/− and AF2° than in old hypertensive wild‐type and C451A mice. Conclusions The nuclear ERα‐AF2 dependent function attenuates angiotensin II–dependent hypertension and protects target organs in aging mice, whereas membrane ERα signaling does not seem to play a role.

scholarly journals Expression of Estrogen Receptor β Is Developmentally Regulated in Reproductive Tissues of Male and Female Mice

2000 ◽  
Vol 62 (2) ◽  
pp. 310-317 ◽  
Author(s):  
Wendy N. Jefferson ◽  
John F. Couse ◽  
Elizabeth Padilla Banks ◽  
Kenneth S. Korach ◽  
Retha R. Newbold
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Developmentally Regulated ◽  
Male And Female ◽  
Female Mice ◽  
Reproductive Tissues

scholarly journals Estrogen Receptor-β Inhibits Skeletal Growth and Has the Capacity to Mediate Growth Plate Fusion in Female Mice

2003 ◽  
Vol 19 (1) ◽  
pp. 72-77 ◽  
Author(s):  
AS Chagin ◽  
MK Lindberg ◽  
N Andersson ◽  
S Moverare ◽  
J-Å Gustafsson ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Growth Plate ◽  
Estrogen Receptor Β ◽  
Skeletal Growth ◽  
Female Mice

scholarly journals Urethral Dysfunction in Female Mice with Estrogen Receptor β Deficiency

PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e109058 ◽  
Author(s):  
Yung-Hsiang Chen ◽  
Chao-Jung Chen ◽  
Shuyuan Yeh ◽  
Yu-Ning Lin ◽  
Yang-Chang Wu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Β ◽  
Female Mice

Estrogen receptor-α mediates estrogen protection from angiotensin II-induced hypertension in conscious female mice

2007 ◽  
Vol 292 (4) ◽  
pp. H1770-H1776 ◽  
Author(s):  
Baojian Xue ◽  
Jaya Pamidimukkala ◽  
Dennis B. Lubahn ◽  
Meredith Hay
Keyword(s):  
Estrogen Receptor ◽  
Angiotensin Ii ◽  
Estrogen Receptor Α ◽  
Protective Role ◽  
Protective Effects ◽  
Pressor Effect ◽  
Ang Ii ◽  
Female Mice ◽  
Female Sex Hormones ◽  
Induced Hypertension

It has been shown that the female sex hormones have a protective role in the development of angiotensin II (ANG II)-induced hypertension. The present study tested the hypotheses that 1) the estrogen receptor-α (ERα) is involved in the protective effects of estrogen against ANG II-induced hypertension and 2) central ERs are involved. Blood pressure (BP) was measured in female mice with the use of telemetry implants. ANG II (800 ng·kg−1·min−1) was administered subcutaneously via an osmotic pump. Baseline BP in the intact, ovariectomized (OVX) wild-type (WT) and ERα knockout (ERαKO) mice was similar; however, the increase in BP induced by ANG II was greater in OVX WT (23.0 ± 1.0 mmHg) and ERαKO mice (23.8 ± 2.5 mmHg) than in intact WT mice (10.1 ± 4.5 mmHg). In OVX WT mice, central infusion of 17β-estradiol (E2; 30 μg·kg−1·day−1) attenuated the pressor effect of ANG II (7.0 ± 0.4 mmHg), and this protective effect of E2 was prevented by coadministration of ICI-182,780 (ICI; 1.5 μg·kg−1·day−1, 18.8 ± 1.5 mmHg), a nonselective ER antagonist. Furthermore, central, but not peripheral, infusions of ICI augmented the pressor effects of ANG II in intact WT mice (17.8 ± 4.2 mmHg). In contrast, the pressor effect of ANG II was unchanged in either central E2-treated OVX ERαKO mice (19.0 ± 1.1 mmHg) or central ICI-treated intact ERαKO mice (19.6 ± 1.6 mmHg). Lastly, ganglionic blockade on day 7 after ANG II infusions resulted in a greater reduction in BP in OVX WT, central ER antagonist-treated intact WT, central E2 + ICI-treated OVX WT, ERαKO, and central E2- or ICI-treated ERαKO mice compared with that in intact WT mice given just ANG II. Together, these data indicate that ERα, especially central expression of the ER, mediates the protective effects of estrogen against ANG II-induced hypertension.

scholarly journals Roles of Phytoestrogen in the Pathophysiology of Intracranial Aneurysm

Stroke ◽  
2021 ◽  
Author(s):  
Kimihiko Yokosuka ◽  
Caleb Rutledge ◽  
Yoshinobu Kamio ◽  
Atsushi Kuwabara ◽  
Hiroki Sato ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Subarachnoid Hemorrhage ◽  
Intracranial Aneurysm ◽  
Protective Effect ◽  
Postmenopausal Women ◽  
Intracranial Aneurysms ◽  
Estrogen Receptor Β ◽  
Systemic Hypertension ◽  
Female Mice ◽  
Aneurysm Formation

Background and Purpose: The incidences of intracranial aneurysm and aneurysmal subarachnoid hemorrhage are high in postmenopausal women. Although population-based studies suggest that hormone replacement therapy is beneficial for postmenopausal women with intracranial aneurysms, estrogen replacement may no longer be recommended for the prevention of chronic diseases given its association with adverse outcomes, such as cancer and ischemic stroke. The isoflavone daidzein and its intestinal metabolite equol are bioactive phytoestrogens and potent agonists of estrogen receptors. Given their estrogenic properties, we investigated whether the isoflavones daidzein and equol are protective against the formation and rupture of intracranial aneurysms in a mouse model of the postmenopausal state. Methods: We induced intracranial aneurysms in ovariectomized adult female mice using a combination of induced systemic hypertension and a single injection of elastase into the cerebrospinal fluid. We fed the mice with an isoflavone-free diet with/without daidzein supplementation, or in a combination of intraperitoneal equol, or oral vancomycin treatment. We also used estrogen receptor beta knockout mice. Results: Both dietary daidzein and supplementation with its metabolite, equol, were protective against aneurysm formation in ovariectomized mice. The protective effects of daidzein and equol required estrogen receptor-β. The disruption of the intestinal microbial conversion of daidzein to equol abolished daidzein’s protective effect against aneurysm formation. Mice treated with equol had lower inflammatory cytokines in the cerebral arteries, suggesting that phytoestrogens modulate inflammatory processes important to intracranial aneurysm pathogenesis. Conclusions: Our study establishes that both dietary daidzein and its metabolite, equol, protect against aneurysm formation in ovariectomized female mice through the activation of estrogen receptor-β and subsequent suppression of inflammation. Dietary daidzein’s protective effect required the intestinal conversion to equol. Our results indicate the potential therapeutic value of dietary daidzein and its metabolite, equol, for the prevention of the formation of intracranial aneurysms and related subarachnoid hemorrhage.

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