Expression of estrogen receptor-α and -β mRNA in the brain of Japanese quail embryos

2007 ◽  
Vol 67 (13) ◽  
pp. 1742-1750 ◽  
Author(s):  
Jeanette Axelsson ◽  
Anna Mattsson ◽  
Björn Brunström ◽  
Krister Halldin
Keyword(s):  
Estrogen Receptor ◽  
Japanese Quail ◽  
Estrogen Receptor Α ◽  
The Brain

Localization of estrogen receptor-α and -βmRNA in brain areas controlling sexual behavior in Japanese quail

2005 ◽  
Vol 66 (2) ◽  
pp. 148-154 ◽  
Author(s):  
Krister Halldin ◽  
Jeanette Axelsson ◽  
Claes Holmgren ◽  
Björn Brunström
Keyword(s):  
Estrogen Receptor ◽  
Sexual Behavior ◽  
Japanese Quail ◽  
Estrogen Receptor Α ◽  
Brain Areas

scholarly journals Estrogen receptor α phosphorylated at Ser216 confers inflammatory function to mouse microglia

2019 ◽  
Author(s):  
Sawako Shindo ◽  
Shih-Heng Chen ◽  
Saki Gotoh ◽  
Kosuke Yokobori ◽  
Hao Hu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Inflammatory Cytokines ◽  
Estrogen Receptor Α ◽  
Microglia Activation ◽  
Immune Functions ◽  
Protein Levels ◽  
Brain Extracts ◽  
Anti Inflammatory ◽  
The Brain ◽  
Pro Inflammatory Cytokines

Abstract Background Estrogen has been suggested to regulate anti-inflammatory signaling in brain microglia through estrogen receptor α (ERα), the only resident immune cells of the brain. The mechanism of how ERα regulates is not well understood. Previously, ERα is phosphorylated at Ser216 in mouse neutrophils, regulating their infiltration into the uterus. Therefore, ERα has now been examined as to its phosphorylation in microglia to regulate their inflammatory functions.MethodsAn antibody against an anti-phospho-S216 peptide of ERα (αP-S216) was used for double immunofluorescence staining to detect to ERα in cultured microglia. A knock-in (KI) mouse line bearing the phosphorylation-blocked ERα mutation S216A (ERα KI) was generated to examine whether this phosphorylation regulate immune functions of microglia.ResultsPhosphorylated ERα at Ser216 was present in microglia but not astrocytes. Staining with an anti-Iba-1 antibody showed that microglia activation was augmented in substantial nigra of ERα KI brains. Lipopolysaccharide (LPS) treatments aggravated microglia activation in ERα KI brains, pro-inflammatory cytokines were increased while anti-inflammatory cytokines were decreased at mRNA and protein levels in whole brain extracts. These increases and decreases of cytokine proteins were also observed in LPS-treated microglia cultured from brains of ERα KI neonates. FACS analysis revealed that ERα KI mutation increased number of IL-6 producing microglia and apoptosis. ERα KI mice decreased motor connection ability in Rotarod tests.ConclusionsBlocking of Ser216 phosphorylation aggravated microglia activation and inflammation of mouse brain, thus confirming that phosphorylated ERα exerts anti-inflammatory functions. ERα KI mice enable us to further investigate the mechanism by which phosphorylated ERα regulates brain immunity and inflammation.

Coumestrol Antagonizes Neuroendocrine Actions of Estrogen via the Estrogen Receptor α

2001 ◽  
Vol 226 (4) ◽  
pp. 301-306 ◽  
Author(s):  
Dena A. Jacob ◽  
Jennifer L. Temple ◽  
Heather B. Patisaul ◽  
Larry J. Young ◽  
Emilie F. Rissman
Keyword(s):  
Estrogen Receptor ◽  
Progesterone Receptors ◽  
Estrogen Receptor Α ◽  
Ventromedial Nucleus ◽  
Wild Type ◽  
Treatment Groups ◽  
Estrogenic Effects ◽  
Low Levels ◽  
The Brain ◽  
All Treatment

The phytoestrogen coumestrol has estrogenic actions on peripheral reproductive tissues. Yet in the brain this compound has both estrogenic and anti-estrogenic effects. We used estrogen receptor α knockout mice (ERαKO) to determine whether coumestrol has estrogenic actions in mice and also if these effects are mediated by the classic ERα. Female wild-type (WT) and ERαKO mice were ovariectomized and treated with estradiol (E2), dietary coumestrol, both, or neither compound. Ten days later the animals were sacrificed, blood was collected, and brain tissues were perfused. Fixed brains were sectioned and immunocytochemistry was employed to quantify progesterone receptors (PR) in the medial preoptic (POA) and ventromedial nucleus of the hypothalamus (VMN). Plasma was assayed for luteinizing hormone (LH). Estrogen treatment induced PR immunoreactivity in both regions in brains of WT females. In ERαKO mice, lower levels of PR were induced. The stimulatory effects of E2 on PR were attenuated in the POA by cotreatment with coumestrol, and the same trend was noted in the VMN. WT ovariectomized females treated with E2 had low levels of LH, while LH was high in untreated females and even higher in ovariectomized females treated with coumestrol. ERαKO females in all treatment groups had high levels of LH. Taken together, the results show that coumestrol has anti-estrogenic actions in the brain and pituitary and that ERα mediates these effects.

scholarly journals Sex Differences in Epigenetic Regulation of the Estrogen Receptor-α Promoter within the Developing Preoptic Area

Endocrinology ◽  
2010 ◽  
Vol 151 (5) ◽  
pp. 2297-2305 ◽  
Author(s):  
Joseph R. Kurian ◽  
Kristin M. Olesen ◽  
Anthony P. Auger
Keyword(s):  
Dna Methylation ◽  
Estrogen Receptor ◽  
Sex Differences ◽  
Preoptic Area ◽  
Estrogen Receptor Α ◽  
Sexually Dimorphic ◽  
Brain And Behavior ◽  
Maternal Interaction ◽  
Methylation Patterns ◽  
The Brain

Sex differences in the brain are largely organized by a testicular hormone surge that occurs in males shortly after birth. Although this hormone surge is transient, sex differences in brain and behavior are lasting. Here we describe a sex difference in DNA methylation of the estrogen receptor-α (ERα) promoter region within the developing rat preoptic area, with males exhibiting more DNA methylation within the ERα promoter than females. More importantly, we report that simulating maternal grooming, a form of maternal interaction that is sexually dimorphic with males experiencing more than females during the neonatal period, effectively masculinizes female ERα promoter methylation and gene expression. This suggests natural variations in maternal care that are directed differentially at males vs. females can influence sex differences in the brain by creating sexually dimorphic DNA methylation patterns. We also find that the early estradiol exposure may contribute to sex differences in DNA methylation patterns. This suggests that early social interaction and estradiol exposure may converge at the genome to organize lasting sex differences in the brain via epigenetic differentiation.

scholarly journals Estrogen receptor α phosphorylated at Ser216 confers inflammatory function to mouse microglia

2020 ◽  
Author(s):  
Sawako Shindo ◽  
Shih-Heng Chen ◽  
Saki Gotoh ◽  
Kosuke Yokobori ◽  
Hao Hu ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Inflammatory Cytokines ◽  
Estrogen Receptor Α ◽  
Brain Diseases ◽  
Antibody Array ◽  
Mouse Uterus ◽  
Glia Cells ◽  
Protein Levels ◽  
Anti Inflammatory ◽  
The Brain

Abstract Background Estrogen receptor α (ERα) has been suggested to regulate anti-inflammatory signaling in brain microglia, the only resident immune cells in the brain. ERα conserves the phosphorylation motif at Ser216 within the DNA binding domain. Previously, Ser216 was found to be phosphorylated in neutrophils infiltrating into the mouse uterus and to enable ERα to regulate migration. Given the implication of this phosphorylation in immune regulation, ERα was examined in mouse microglia to determine if Ser216 is phosphorylated and regulates microglia’s inflammation. It was found that Ser216 was constitutively phosphorylated in microglia and demonstrated that in the absence of phosphorylated ERα in ERα KI brains microglia inflamed, confirming that phosphorylation confers ERα with anti-inflammatory capability. ERα KI mice were obese and weakened motor ability. Methods Mixed glia cells were prepared from brains of 2-days-old neonates and cultured to mature and isolate microglia. An antibody against an anti-phospho-S216 peptide of ERα (αP-S216) was used to detect phosphorylated ERα in double immunofluorescence staining with ERα antibodies and a microglia maker Iba-1 antibody. A knock-in (KI) mouse line bearing the phosphorylation-blocked ERα S216A mutation (ERα KI) was generated to examine inflammation-regulating functions of phosphorylated ERα in microglia. RT-PCR, antibody array, ELISA and FACS assays were employed to measure expressions of pro- or anti-inflammatory cytokines at their mRNA and protein levels. Rotarod tests were performed to examine motor connection ability.Results Double immune staining of mixed glia cells showed that ERα is phosphorylated at Ser216 in microglia, but not astrocytes. Immunohistochemistry with an anti-Iba-1 antibody showed that microglia cells were swollen and shortened branches in the substantial nigra (SN) of ERα KI brains, indicating the spontaneous activation of microglia as observed with those of lipopolysaccharide (LPS)-treated ERα WT brains. Pro-inflammatory cytokines were up-regulated in the brain of ERα KI brains as well as cultured microglia, whereas anti-inflammatory cytokines were down-regulated. FACS analysis showed that the number of IL-6 producing and apoptotic microglia increased in those prepared from ERα KI brains. Times of ERα KI mice on rod were shortened in Rotarod tests. Conclusions Blocking of Ser216 phosphorylation aggravated microglia activation and inflammation of mouse brain, thus confirming that phosphorylated ERα exerts anti-inflammatory functions. ERα KI mice enable us to further investigate the mechanism by which phosphorylated ERα regulates brain immunity and inflammation and brain diseases.

scholarly journals cDNA Cloning and mRNA Expression of Estrogen Receptor α in Japanese Quail

2003 ◽  
Vol 40 (2) ◽  
pp. 121-129 ◽  
Author(s):  
Kouhei Ichikawa ◽  
Ichiro Yamamoto ◽  
Akira Tsukada ◽  
Noboru Saito ◽  
Kiyoshi Shimada
Keyword(s):  
Estrogen Receptor ◽  
Mrna Expression ◽  
Cdna Cloning ◽  
Japanese Quail ◽  
Estrogen Receptor Α

Glucoprivation increases estrogen receptor α immunoreactivity in the brain catecholaminergic neurons in ovariectomized rats

2001 ◽  
Vol 299 (1-2) ◽  
pp. 109-112 ◽  
Author(s):  
Beverly A.S Reyes ◽  
Maria Amelita C Estacio ◽  
Helen I'Anson ◽  
Hiroko Tsukamura ◽  
Kei-ichiro Maeda
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Ovariectomized Rats ◽  
Catecholaminergic Neurons ◽  
The Brain

scholarly journals Soy Isoflavone Supplements Antagonize Reproductive Behavior and Estrogen Receptor α- and β-Dependent Gene Expression in the Brain*

Endocrinology ◽  
2001 ◽  
Vol 142 (7) ◽  
pp. 2946-2952 ◽  
Author(s):  
Heather B. Patisaul ◽  
Marietta Dindo ◽  
Patricia L. Whitten ◽  
Larry J. Young
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Reproductive Behavior ◽  
Estrogen Receptor Α ◽  
Soy Isoflavone ◽  
The Brain
Sign in / Sign up

Export Citation Format

Share Document