scholarly journals Biologically Active Estrogen Receptor-β: Evidence from in Vivo Autoradiographic Studies with Estrogen Receptor α-Knockout Mice

Endocrinology ◽  
1999 ◽  
Vol 140 (6) ◽  
pp. 2613-2620 ◽  
Author(s):  
Paul J. Shughrue ◽  
Malcolm V. Lane ◽  
Istvan Merchenthaler
Keyword(s):  
Estrogen Receptor ◽  
Knockout Mice ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Β ◽  
Biologically Active

scholarly journals Regulation of Postnatal Lung Development and Homeostasis by Estrogen Receptor β

2003 ◽  
Vol 23 (23) ◽  
pp. 8542-8552 ◽  
Author(s):  
Cesare Patrone ◽  
Tobias N. Cassel ◽  
Katarina Pettersson ◽  
Yun-Shang Piao ◽  
Guojun Cheng ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Adult Female ◽  
Lung Development ◽  
Estrogen Receptor Α ◽  
Biologically Active ◽  
Gm Csf ◽  
Postnatal Lung Development ◽  
Alveolar Formation

ABSTRACT Estrogens have well-documented effects on lung development and physiology. However, the classical estrogen receptor α (ERα) is undetectable in the lung, and this has left many unanswered questions about the mechanism of estrogen action in this organ. Here we show, both in vivo and in vitro, that ERβ is abundantly expressed and biologically active in the lung. Comparisons of lungs from wild-type mice and mice with an inactivated ERβ gene (ERβ−/−) revealed decreased numbers of alveoli in adult female ERβ−/− mice and findings suggesting deficient alveolar formation as well as evidence of surfactant accumulation. Platelet-derived growth factor A (PDGF-A) and granulocyte-macrophage colony-stimulating factor (GM-CSF), key regulators of alveolar formation and surfactant homeostasis, respectively, were decreased in lungs of adult female ERβ−/− mice, and direct transcriptional regulation of these genes by ERβ was demonstrated. This suggests that estrogens act via ERβ in the lung to modify PDGF-A and GM-CSF expression. These results provide a potential molecular mechanism for the gender differences in alveolar structure observed in the adult lung and establish ERβ as a previously unknown regulator of postnatal lung development and homeostasis.

Morphological Studies of Prolactin-Secreting Cells in Estrogen Receptor α and Estrogen Receptor β Knockout Mice

2003 ◽  
Vol 77 (5) ◽  
pp. 324-333 ◽  
Author(s):  
Georges Pelletier ◽  
Songyun Li ◽  
Daniel Phaneuf ◽  
Céline Martel ◽  
Fernand Labrie
Keyword(s):  
Estrogen Receptor ◽  
Knockout Mice ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Β ◽  
Morphological Studies

scholarly journals Deletion of estrogen receptor α in skeletal muscle results in impaired contractility in female mice

2018 ◽  
Vol 124 (4) ◽  
pp. 980-992 ◽  
Author(s):  
Brittany C. Collins ◽  
Tara L. Mader ◽  
Christine A. Cabelka ◽  
Melissa R. Iñigo ◽  
Espen E. Spangenburg ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Estrogen Receptor ◽  
Muscle Strength ◽  
Body Mass ◽  
Light Chain ◽  
Knockout Mice ◽  
Contractile Function ◽  
Estrogen Receptor Α ◽  
Myosin Regulatory Light Chain

Estradiol deficiency in females can result in skeletal muscle strength loss, and treatment with estradiol mitigates the loss. There are three primary estrogen receptors (ERs), and estradiol elicits effects through these receptors in various tissues. Ubiquitous ERα-knockout mice exhibit numerous biological disorders, but little is known regarding the specific role of ERα in skeletal muscle contractile function. The purpose of this study was to determine the impact of skeletal muscle-specific ERα deletion on contractile function, hypothesizing that ERα is a main receptor through which estradiol affects muscle strength in females. Deletion of ERα specifically in skeletal muscle (skmERαKO) did not affect body mass compared with wild-type littermates (skmERαWT) until 26 wk of age, at which time body mass of skmERαKO mice began to increase disproportionally. Overall, skmERαKO mice had low strength demonstrated in multiple muscles and by several contractile parameters. Isolated extensor digitorum longus muscles from skmERαKO mice produced 16% less eccentric and 16–26% less submaximal and maximal isometric force, and isolated soleus muscles were more fatigable, with impaired force recovery relative to skmERαWT mice. In vivo maximal torque productions by plantarflexors and dorsiflexors were 16% and 12% lower in skmERαKO than skmERαWT mice, and skmERαKO muscles had low phosphorylation of myosin regulatory light chain. Plantarflexors also generated 21–32% less power, submaximal isometric and peak concentric torques. Data support the hypothesis that ablation of ERα in skeletal muscle results in muscle weakness, suggesting that the beneficial effects of estradiol on muscle strength are receptor mediated through ERα. NEW & NOTEWORTHY We comprehensively measured in vitro and in vivo skeletal muscle contractility in female estrogen receptor α (ERα) skeletal muscle-specific knockout mice and report that force generation is impaired across multiple parameters. These results support the hypothesis that a primary mechanism through which estradiol elicits its effects on strength is mediated by ERα. Evidence is presented that estradiol signaling through ERα appears to modulate force at the molecular level via posttranslational modifications of myosin regulatory light chain.

1322: The Expression of Estrogen Receptor α and Estrogen Receptor β in the Human Fetal Prostate

2004 ◽  
Vol 171 (4S) ◽  
pp. 348-348
Author(s):  
Ellen Shapiro ◽  
Hongying Huang ◽  
Rachael R. Mash ◽  
Eliza Ng ◽  
Deborah E. McFadden ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Β

scholarly journals Mouse Estrogen Receptor β Forms Estrogen Response Element-Binding Heterodimers with Estrogen Receptor α

1997 ◽  
Vol 11 (10) ◽  
pp. 1486-1496 ◽  
Author(s):  
Katarina Pettersson ◽  
Kaj Grandien ◽  
George G. J. M. Kuiper ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Receptor Β ◽  
Estrogen Response Element ◽  
Response Element ◽  
Estrogen Response

Multiple forms of estrogen receptor-α in cerebral blood vessels: regulation by estrogen

2003 ◽  
Vol 284 (1) ◽  
pp. E184-E192 ◽  
Author(s):  
Chris Stirone ◽  
Sue P. Duckles ◽  
Diana N. Krause
Keyword(s):  
Estrogen Receptor ◽  
Blood Vessels ◽  
Estrogen Receptor Α ◽  
26S Proteasome ◽  
Target Tissue ◽  
Female Rat ◽  
Cerebral Vasculature ◽  
Cerebral Blood Vessels ◽  
Multiple Forms

The cerebral vasculature is an important target tissue for estrogen, as evidenced by significant effects of estrogen on vascular reactivity and protein levels of endothelial nitric oxide synthase and prostacyclin synthase. However, the presence, localization, and regulation of estrogen receptors in the cerebral vasculature have not been investigated. In this study, we identified the presence of estrogen receptor-α (ER-α) in female rat cerebral blood vessels and localized this receptor to both smooth muscle and endothelial cells by use of immunohistochemistry and confocal microscopy. With immunoblot analysis, multiple forms of ER-α were detected at 110, 93, 82, 50, and 45 kDa in addition to a relatively weak band corresponding to the 66-kDa putative unmodified receptor. The 82-kDa band was identified as Ser118-phosphorylated ER-α, whereas the 50-kDa band lacks the normal NH2 terminus, suggestive of an ER-α splice variant. Lower molecular mass bands persisted after in vivo inhibition of 26S proteasome activity with lactacystin, whereas the 110- and 93-kDa bands increased. All forms of ER-α in cerebral vessels were decreased after ovariectomy but significantly increased after chronic estrogen exposure in vivo.

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