scholarly journals Expression of Estrogen Receptor α and β in Rat Astrocytes in Primary Culture: Effects of Hypoxia and Glucose Deprivation

2011 ◽  
pp. 951-960 ◽  
Author(s):  
M. D. AL-BADER ◽  
S. A. MALATIALI ◽  
Z. B. REDZIC
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Biological Effects ◽  
Estrogen Receptor Beta ◽  
Glucose Deprivation ◽  
Estrogen Receptor Α ◽  
Full Length ◽  
Control Group ◽  
Rat Astrocyte

Estrogen replacement therapy could play a role in the reduction of injury associated with cerebral ischemia in vivo, which could be, at least partially, a consequence of estrogen influence of glutamate buffering by astrocytes during hypoxia/ischemia. Estrogen exerts biological effects through interaction with its two receptors: estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ), which are both expressed in astrocytes. This study explored effects of hypoxia and glucose deprivation (HGD), alone or followed by 1 h recovery, on ERα and ERβ expression in primary rat astrocyte cultures following 1 h exposure to: a) 5 % CO2 in air (control group-CG); b) 2 % O2/5 % CO2 in N2 with glucose deprivation (HGD group-HGDG); or c) the HGDG protocol followed by 1 h CG protocol (recovery group-RG). ERα mRNA expression decreased in HGDG. At the protein level, full-length ERα (67 kDa) and three ERα-immunoreactive protein bands (63, 60 and 52 kDa) were detected. A significant decrease in the 52 kDa band was seen in HGDG, while a significant decrease in expression of the full length ERα was seen in the RG. ERβ mRNA and protein expression (a 54 kDa single band) did not change. The observed decrease in ERα protein may limit estrogen-mediated signalling in astrocytes during hypoxia and recovery.

scholarly journals 3,3′-Diindolylmethane Dose-Dependently Prevents Advanced Prostate Cancer

2019 ◽  
Author(s):  
Yufei Li ◽  
Nathaniel W. Mahloch ◽  
Nicholas J.E. Starkey ◽  
Mónica Peña-Luna ◽  
George E. Rottinghaus ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Estrogen Receptor ◽  
High Fat Diet ◽  
Estrogen Receptor Alpha ◽  
Estrogen Receptor Beta ◽  
Control Group ◽  
High Fat ◽  
Mouse Prostate

Abstract3,3′-Diindolylmethane (DIM) is an acid-derived dimer of indole-3-carbinol, found in many cruciferous vegetables, such as broccoli, and has been shown to inhibit prostate cancer (PCa) in several in vitro and in vivo models. We demonstrated that DIM stimulated both estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) transcriptional activities and propose that ERβ plays a role in mediating DIM’s inhibition on cancer cell growth. To further study the effects of DIM on inhibiting advanced PCa development, we tested DIM in TRAMP (TRansgenic Adenocarcinoma of the Mouse Prostate) mice. The control group of mice were fed a high fat diet. Three additional groups of mice were fed the same high fat diet supplemented with 0.04%, 0.2% and 1% DIM. Incidence of advanced PCa, poorly differentiated carcinoma (PDC), in the control group was 60%. 1% DIM dramatically reduced PDC incidence to 24% (p=0.0012), while 0.2% and 0.04% DIM reduced PDC incidence to 38% (p=0.047) and 45% (p=0.14) respectively. Though DIM did affect mice weights, statistical analysis showed a clear negative association between DIM concentration and PDC incidence with p=0.004, while the association between body weight and PDC incidence was not significant (p=0.953). In conclusion, our results show that dietary DIM can inhibit the most aggressive stage of prostate cancer at concentration lower than previously demonstrated, possibly working through an estrogen receptor mediated mechanism.

Abstract P130: Estrogen Receptor β Mediates the Rescue of Cardiac Function in Advanced Heart Failure by Promoting Neoangiogenesis and Reducing Fibrosis

2011 ◽  
Vol 109 (suppl_1) ◽  
Author(s):  
Andrea Iorga ◽  
Rod Partow-Navid ◽  
Humann Matori ◽  
Jingyuan Li ◽  
Soban Umar ◽  
...  
Keyword(s):  
Heart Failure ◽  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Cardiac Fibrosis ◽  
Biological Effects ◽  
Estrogen Receptor Beta ◽  
Pressure Overload ◽  
Decompensated Heart Failure ◽  
Beta Agonist ◽  
Receptor Beta

Estrogen can act via the estrogen receptor alpha (ERa) or estrogen receptor beta (ERb) to exert its biological effects, and both of these receptors are present in the heart. We have previously shown that short-term estrogen (E2) treatment can rescue pressure overload-induced decompensated heart failure (HF) in mice, and that this rescue is achieved mainly through the ERb. Furthermore, E2 has been shown to regulate angiogenesis in different tissues. Because HF has been associated with decreased angiogenesis and increased fibrosis, here we investigated whether the E2-induced rescue of HF by the selective ERb agonist DPN can regulate cardiac fibrosis and neoangiogenesis. We used transaortic constriction to induce HF, and once the ejection fraction (EF) reached ∼30%, one group of animals was sacrificed (HF group), and the other three groups received either 17b-estradiol via a subcutaneous pellet implant (0.012mg/pellet, n=16), selective ERa agonist (PPT, 0.625mg/kg/day), or selective ERb agonist (DPN, 0.625mg/kg/day) for 10 days. Serial echocardiography was performed to monitor cardiac structure and function. As expected, E2 rescued HF by restoring EF from 33.17±1.12% to 53.05±1.29%. Mice treated with DPN had a significant EF improvement from 33.17±1.12% to 45.25±2.1% (n=7), while the EF of PPT-treated mice did not improve (31.09±2.3%, n=6). Similarly, only the fractional shortening of DPN-treated mice improved from 15.7±0.58% in HF to 21.95±1.65% with DPN treatment vs. 14.72±1.24% with PPT. Next, we examined whether promotion of cardiac neoangiogenesis and suppression of fibrosis by the selective ERb agonist are possible mechanisms in the rescue action of HF by DPN. DPN treatment was able to reverse the interstitial and perivascular fibrosis observed in HF, while PPT had no effect. The selective ERb agonist also stimulated neoangiogenesis, as the capillary density was increased from 0.46±0.04 microvessels/cardiomyocyte in HF to 0.67±0.07 with DPN treatment, whereas PPT treatment had no effect (0.43±0.03). Our data strongly suggests that upregulation of cardiac neoangiogenesis and reversal of fibrosis are pivotal mechanisms in rescuing advanced HF by the estrogen receptor beta agonist DPN.

scholarly journals Correlations between Low Doses of Zearalenone, Its Carryover Factor and Estrogen Receptor Expression in Different Segments of the Intestines in Pre-Pubertal Gilts—A Study Protocol

Toxins ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 379
Author(s):  
Magdalena Gajęcka ◽  
Magdalena Mróz ◽  
Paweł Brzuzan ◽  
Ewa Onyszek ◽  
Łukasz Zielonka ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mrna Expression ◽  
Estrogen Receptor Beta ◽  
Receptor Expression ◽  
Control Group ◽  
Plant Materials ◽  
Expression Of Genes ◽  
Horizontal Part

Plant materials can be contaminated with Fusarium mycotoxins and their derivatives, whose toxic effects on humans and animals may remain subclinical. Zearalenone (ZEN), a low-molecular-weight compound, is produced by molds in crop plants as a secondary metabolite. The objective of this study will be to analyze the in vivo correlations between very low monotonic doses of ZEN (5, 10, and 15 μg ZEN/kg body weight—BW for 42 days) and the carryover of this mycotoxin and its selected metabolites from the intestinal contents to the intestinal walls, the mRNA expression of estrogen receptor alfa (ERα) and estrogen receptor beta (ERβ) genes, and the mRNA expression of genes modulating selected colon enzymes (CYP1A1 and GSTP1) in the intestinal mucosa of pre-pubertal gilts. An in vivo experiment will be performed on 60 clinically healthy animals with initial BW of 14.5 ± 2 kg. The gilts will be randomly divided into a control group (group C, n = 15) and three experimental groups (group ZEN5, group ZEN10, and group ZEN15; n = 15). Group ZEN5 will be administered per os 5 μg ZEN/kg BW (MABEL), group ZEN10—10 μg ZEN/kg BW (NOAEL), and group ZEN15—15 µg ZEN/kg BW (low LOAEL). In each group, five animals will be euthanized on analytical dates 1 (exposure day 7), 2 (exposure day 21), and 3 (exposure day 42). Samples for in vitro analyses will be collected from an intestinal segment resected from the following regions: the third (horizontal) part of the duodenum, jejunum, ileum, cecum, ascending colon, transverse colon, and descending colon. The experimental material will be collected under special conditions, and it will be transported to specialist laboratories where samples will be obtained for further analyses.

Implications of estrogen receptor alpha and estrogen receptor beta for adipose tissue functions and cardiometabolic complications

2013 ◽  
Vol 15 (3) ◽  
Author(s):  
Hui Gao ◽  
Karin Dahlman-Wright
Keyword(s):  
Estrogen Receptor ◽  
Adipose Tissue ◽  
Estrogen Receptor Alpha ◽  
Molecular Mechanisms ◽  
Estrogen Receptor Beta ◽  
Estrogen Receptor Α ◽  
Endocrine Function ◽  
Estrogen Signaling ◽  
Strongly Connected

AbstractThere is growing evidence that estrogen signaling regulates energy metabolism and exerts important functions in maintaining adipose tissue metabolism, including controlling the distribution of body fat. Changes in the physiological functions of adipose tissue, particularly the white adipose tissue, have been strongly connected to obesity and the development of related cardiometabolic complications. In this review, we will focus on discussing the role of estrogen signaling in regulating adipocyte differentiation, metabolism and its endocrine function with a focus on the possible underlying molecular mechanisms mediated by estrogen receptor α and estrogen receptor β.

scholarly journals Protective Hematopoietic Effect of Estrogens in a Mouse Model of Thrombosis: Respective Roles of Nuclear Versus Membrane Estrogen Receptor α

Endocrinology ◽  
2015 ◽  
Vol 156 (11) ◽  
pp. 4293-4301 ◽  
Author(s):  
Marie-Cécile Valéra ◽  
Coralie Fontaine ◽  
Françoise Lenfant ◽  
Cendrine Cabou ◽  
Maeva Guillaume ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Bleeding Time ◽  
Activation Function ◽  
Estrogen Receptor Α ◽  
Loss Of Function ◽  
Antithrombotic Effects ◽  
17Β Estradiol ◽  
First Time

We recently reported that chronic 17β-estradiol (E2) treatment in mice decreases platelet responsiveness, prolongs the tail-bleeding time and protects against acute thromboembolism via the hematopoietic estrogen receptor alpha (ERα), and independently of ERβ. Here, we have explored the respective roles of membrane vs nuclear actions of ERα in this process, using: 1) the selective activator of membrane ERα: estrogen dendrimer conjugate, and 2) mouse models with mutations in ERα. The selective targeting of activation function 2 of ERα provides a model of nuclear ERα loss-of-function, whereas mutation of the ERα palmitoylation site leads to a model of membrane ERα deficiency. The combination of pharmacological and genetic approaches including hematopoietic chimera mice demonstrated that absence of either membrane or nuclear ERα activation in bone marrow does not prevent the prolongation of the tail-bleeding time, suggesting a redundancy of these two functions for this E2 effect. In addition, although hematopoietic membrane ERα is neither sufficient nor necessary to protect E2-treated mice from collagen/epinephrine-induced thromboembolism, the protection against death-induced thromboembolism is significantly reduced in the absence of hematopoietic nuclear ERα activation. Overall, this study emphasizes that hematopoietic cells (likely megakaryocytes and possibly immune cells) constitute an important target in the antithrombotic effects of estrogens, and delineate for the first time in vivo the respective roles of membrane vs nuclear ERα effects, with a prominent role of the latter.

scholarly journals Expression of Estrogen Receptor α by Decidual Macrophages in Preeclampsia

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 191 ◽  
Author(s):  
Polina Vishnyakova ◽  
Anastasiya Poltavets ◽  
Maria Nikitina ◽  
Konstantin Midiber ◽  
Liudmila Mikhaleva ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Late Onset ◽  
Normal Pregnancy ◽  
Estrogen Receptor Α ◽  
Control Group ◽  
Tissue Fluid ◽  
Tissue Samples ◽  
Cultural Methods ◽  
Anti Inflammatory ◽  
Early Onset Preeclampsia

Preeclampsia is a gestation-associated hypertensive syndrome that threatens the life and health of the mother and the child. The condition is presumably caused by systemic failure with a strong involvement of innate immunity. In particular, it has been associated with flexible phenotypes of macrophages, which depend on the molecules circulating in the blood and tissue fluid, such as cytokines and hormones. This study aimed at a comparative evaluation of pro-inflammatory (TNFα) and anti-inflammatory (CD206, MMP9, HGF) markers, as well as the levels of estrogen receptor α, expressed by decidual macrophages in normal pregnancy and in patients with early- and late-onset preeclampsia. The tissue samples of decidua basalis were examined by immunohistochemistry and Western blotting. Isolation of decidual macrophages and their characterization were performed using cultural methods, flow cytometry and real-time PCR. Over 50% of the isolated decidual macrophages were positive for the pan-macrophage marker CD68. In the early-onset preeclampsia group, the levels of estrogen receptor α in decidua were significantly decreased. Furthermore, significantly decreased levels of HGF and CD206 were observed in both preeclampsia groups compared with the control group. The observed downregulation of estrogen receptor α, HGF and CD206 may contribute to the balance of pro- and anti-inflammatory macrophages and thereby to pathogenesis of preeclampsia.

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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