scholarly journals Estradiol Stimulates Apolipoprotein A-IV Gene Expression in the Nucleus of the Solitary Tract Through Estrogen Receptor-α

Endocrinology ◽  
2014 ◽  
Vol 155 (10) ◽  
pp. 3882-3890 ◽  
Author(s):  
Ling Shen ◽  
Yin Liu ◽  
David Q.H. Wang ◽  
Patrick Tso ◽  
Stephen C. Woods ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Nucleus Tractus Solitarius ◽  
Body Weight Gain ◽  
Gene Promoter ◽  
Estrogen Receptor Α ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Upstream Region ◽  
Apolipoprotein A

Abstract Although estrogens have been implicated in the regulation of apolipoprotein A-IV (apo A-IV) gene expression in the nucleus tractus solitarius, previous studies have not defined the molecular mechanism. The aim of this study was to examine the transcriptional mechanisms involved in regulation of apo A-IV gene expression. Using cultured primary neuronal cells from rat embryonic brainstems, we found that treatment with 10nM 17β-estradiol-3-benzoate (E2) or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol (an estrogen receptor [ER]α agonist), but not 2,3-bis(4-hydroxyphenyl)-propionitrile (an ERβ agonist), significantly increased apo A-IV gene expression, compared with vehicle treatment. This effect of E2 was abolished when the cells were incubated with E2 linked to BSA, which prevents E2 from entering cells, implying that a nongenomic mechanism of E2 is not involved. Two putative estrogen response elements were identified at the 5′-upstream region of the apo A-IV gene promoter, but only 1 of them was able to recruit ERα, leading to increased apo A-IV gene expression, as determined by chromatin immunoprecipitation assay and luciferase activity analysis. A cyclic regimen of E2 or 4,4′,4″-(4-propyl-[1H]-pyrazole-1,3,5-triyl) trisphenol treatment for 8 cycles (4 d/cycle, mimicking the ovarian cycle of female rats) in ovariectomized female rats significantly reduced food intake and body weight gain and increased apo A-IV gene expression in the nucleus tractus solitarius, relative to vehicle. These data collectively demonstrate that nuclear ERα is the primary mediator of E2's action on apo A-IV gene expression and suggest that increased signaling of endogenous apo A-IV may at least partially mediate E2-induced inhibitory effect on feeding.

scholarly journals Estradiol Increases the Anorectic Effect of Central Apolipoprotein A-IV

Endocrinology ◽  
2010 ◽  
Vol 151 (7) ◽  
pp. 3163-3168 ◽  
Author(s):  
Ling Shen ◽  
David Q.-H. Wang ◽  
Chun-min Lo ◽  
Patrick Tso ◽  
W. Sean Davidson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Estrogen Receptor Α ◽  
Inhibitory Effect ◽  
Estradiol Treatment ◽  
Apolipoprotein A ◽  
Ovx Rats ◽  
Anorectic Effect

Estrogens have potent suppressive effects on food intake and body weight in many species, including humans. Compelling evidence suggests estrogen’s anorectic action is through an indirect mechanism by enhancing the strength of other physiological signals that reduce meal size such as apolipoprotein A-IV (apo A-IV), a satiation factor from the gut and brain. We determined whether estradiol, the primary form of estrogen, modulates the anorectic effect of apo A-IV. Intrafourth ventricular administration of low doses of apo A-IV reduced food intake to a greater extent in ovariectomized (OVX) rats cyclically treated with estradiol than in vehicle-treated OVX controls, implying that cyclic estradiol replacement increases the satiating potency of apo A-IV. OVX significantly increased food intake and body weight but decreased apo A-IV gene expression in the nucleus tractus solitarius (NTS). All of these alterations were reversed by cyclic regimen of estradiol treatment. The finding of colocalization of apo A-IV with estrogen receptor-α in the NTS suggests that estradiol might act locally in the NTS to up-regulate apo A-IV gene expression. Finally, OVX apo A-IV knockout mice had a smaller feeding response to estradiol because they ate significantly more food and gained more body weight than OVX wild-type controls during the period of cyclic estradiol replacement. These data indicate that an increased signaling of endogenous apo A-IV may partially mediate estradiol-induced inhibitory effect on feeding.

scholarly journals Neonatal Exposure to Bisphenol A Alters Rat Uterine Implantation-Associated Gene Expression and Reduces the Number of Implantation Sites

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1101-1111 ◽  
Author(s):  
Jorgelina Varayoud ◽  
Jorge G. Ramos ◽  
Verónica L. Bosquiazzo ◽  
Melina Lower ◽  
Mónica Muñoz-de-Toro ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Bisphenol A ◽  
Steroid Receptors ◽  
Estrogen Receptor Α ◽  
Receptor Expression ◽  
Female Rats ◽  
Postnatal Exposure ◽  
Long Term Effects ◽  
Implantation Sites

Endocrine disrupters have been associated with reproductive pathologies such as infertility and gynecological tumors. Using a rat model of early postnatal exposure to bisphenol A (BPA), we evaluated the long-term effects on 1) female reproductive performance, 2) uterine homeobox A10 (Hoxa10) and Hoxa10-target gene expression, and 3) ovarian steroid levels and uterine estrogen receptor α and progesterone (P) receptor expression. Newborn female rats received vehicle, BPA.05 (0.05 mg/kg · d), BPA20 (20 mg/kg · d), diethylstilbestrol.2 (0.2 μg/kg · d), or diethylstilbestrol 20 (20 μg/kg · d) on postnatal d 1, 3, 5, and 7. A significant decrease in the number of implantation sites was assessed in the xenoestrogen-exposed females. To address the molecular effects of postnatal xenoestrogen exposure on the pregnant uterus, we evaluated the expression of implantation-associated genes on d 5 of pregnancy (preimplantation uterus). All xenoestrogen-treated rats showed a lower expression of Hoxa10. In the same animals, two Hoxa10-downstream genes were misregulated in the uterus. β3Integrin, which is up-regulated by Hoxa10 in controls, was decreased, whereas empty spiracles homolog 2, which is down-regulated by Hoxa10, was increased. Furthermore a clear down-regulation of estrogen receptor α and P receptor expression was detected without changes in estradiol and P serum levels. The early exposure to BPA produced a lower number of implantation sites in association with a defective uterine environment during the preimplantation period. Alterations in the endocrine-regulated Hoxa10 gene pathways (steroid receptors—Hoxa10—β3integrin/empty spiracles homolog 2) could explain, at least in part, the BPA effects on the implantation process.

scholarly journals Loading-related regulation of gene expression in bone in the contexts of estrogen deficiency, lack of estrogen receptor α and disuse

Bone ◽  
2010 ◽  
Vol 46 (3) ◽  
pp. 628-642 ◽  
Author(s):  
Gul Zaman ◽  
Leanne K. Saxon ◽  
Andrew Sunters ◽  
Helen Hilton ◽  
Peter Underhill ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Regulation Of Gene Expression ◽  
Estrogen Receptor Α ◽  
Estrogen Deficiency

scholarly journals Estrogen Receptor α Gene Promoter 0/B Usage in the Rat Sexually Dimorphic Nucleus of the Preoptic Area

Endocrinology ◽  
2010 ◽  
Vol 151 (4) ◽  
pp. 1923-1928 ◽  
Author(s):  
Tomohiro Hamada ◽  
Yasuo Sakuma
Keyword(s):  
Estrogen Receptor ◽  
Sexual Differentiation ◽  
Preoptic Area ◽  
Gene Promoter ◽  
Estrogen Receptor Α ◽  
Egfp Expression ◽  
Sexually Dimorphic ◽  
Transgenic Rats ◽  
The Core ◽  
Sexually Dimorphic Nucleus

The volume of the sexually dimorphic nucleus of the preoptic area (SDN-POA) is two to four times larger in male rats than in females; however, the mechanism for the establishment of sexual dimorphism and the function of this nucleus is almost unknown. Perinatal estrogen can cause sexual dimorphism via the estrogen receptor α (ERα). Recently, transgenic rats were generated that express enhanced green fluorescent protein (EGFP) under the control of the ERα gene promoter 0/B to tag ERα-positive neurons in the brain. In the present study, we examined whether this EGFP expression could be a marker for the SDN-POA in adults. EGFP-labeled cells were distributed in the core of the SDN-POA (0/B-SDN) of male and female transgenic rats, in accordance with the Nissl staining and immunoreactivity for the SDN marker, calbindin. They were also immunoreactive for ERα. The core was bigger in volume and contained more 0/B-SDN neurons in males than in females. The EGFP-tagged cells were packed more densely in the female core than that in males. Subcutaneous injection of 100 μg 17β-estradiol to females on the day of birth, or orchidectomy of male neonates, reversed the sexually dimorphic phenotype of the volume of the 0/B-SDN, despite not affecting the cell number. We suggest that this EGFP expression in the SDN-POA could be a useful marker to clarify the sexual differentiation and function of the SDN-POA. Moreover, the ERα gene promoter 0/B plays a key role in the organization of the sexual differentiation of the SDN-POA.

G-protein Coupled Estrogen Receptor Expression in Growth Hormone Secreting and Non-Functioning Adenomas

2020 ◽  
Author(s):  
Hande Mefkure Ozkaya ◽  
Muge Sayitoglu ◽  
Nil Comunoglu ◽  
Eda Sun ◽  
Fatma Ela Keskin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Protein Expression ◽  
G Protein ◽  
Estrogen Receptor Α ◽  
Receptor Expression ◽  
Positive Correlation ◽  
Polymerase Chain ◽  
G Protein Coupled ◽  
Transforming Gene

Abstract Purpose To evaluate the expression of G-protein coupled estrogen receptor (GPER1), aromatase, estrogen receptor α (ERα), estrogen receptor β (ERβ), pituitary tumor transforming gene (PTTG), and fibroblast growth factor 2 (FGF2) in GH-secreting and non-functioning adenomas (NFA). Methods Thirty patients with acromegaly and 27 patients with NFA were included. Gene expression was determined via quantitative reverse transcription polymerase chain reaction (QRT-PCR). Protein expression was determined via immunohistochemistry. Results There was no difference, in terms of gene expression of aromatase, ERα, PTTG, and FGF2 between the two groups (p>0.05 for all). ERβ gene expression was higher and GPER1 gene expression was lower in GH-secreting adenomas than NFAs (p<0.05 for all). Aromatase and ERβ protein expression was higher in GH-secreting adenomas than NFAs (p=0.01). None of the tumors expressed ERα. GPER1 expression was detected in 62.2% of the GH-secreting adenomas and 45% of NFAs. There was no difference in terms of GPER1, PTTG, FGF2 H scores between the two groups (p>0.05 for all). GPER1 gene expression was positively correlated to ERα, ERβ, PTTG, and FGF2 gene expression (p<0.05 for all). There was a positive correlation between aromatase and GPER1 protein expression (r=0.31; p=0.04). Conclusions GPER1 is expressed at both gene and protein level in a substantial portion of GH-secreting adenomas and NFAs. The finding of a positive correlation between GPER1 and ERα, ERβ, PTTG, and FGF2 gene expression and aromatase and GPER1 protein expression suggests GPER1 along with aromatase and classical ERs might mediate the effects of estrogen through upregulation of PTTG and FGF2.

Sites of action of testosterone and estradiol on longitudinal bone growth

1983 ◽  
Vol 244 (2) ◽  
pp. E135-E140 ◽  
Author(s):  
J. O. Jansson ◽  
S. Eden ◽  
O. Isaksson
Keyword(s):  
Replacement Therapy ◽  
Bone Growth ◽  
Body Weight Gain ◽  
Inhibitory Effect ◽  
Body Growth ◽  
Female Rats ◽  
Male Rats ◽  
Longitudinal Bone Growth ◽  
Sites Of Action ◽  
Different Doses

In this study the mechanisms by which sex steroids influence body growth were investigated. The effect of different doses of testosterone propionate on longitudinal bone growth and body weight gain was studied in a) gonadectomized male rats, b) gonadohypophysectomized male rats, and c) gonadohypophysectomized male rats given replacement therapy with bovine growth hormone (bGH). The effect of different doses of estradiol benzoate on the same growth parameters was studied in female rats divided into the same experimental groups as the males. Accumulated longitudinal bone growth was determined using oxytetracycline as an intravital marker. Testosterone caused a dose-dependent increase in longitudinal bone growth in gonadectomized male rats. In contrast, testosterone exerted no significant increase in longitudinal bone growth in gonadohypophysectomized male rats with and without bGH replacement therapy. Treatment with estrogen inhibited longitudinal bone growth and body weight gain. The inhibitory effect of estradiol was approximately the same in gonadohypophysectomized female rats given bGH replacement therapy as in gonadectomized female rats. The results suggest that testosterone exerts its stimulatory effect on body growth mainly by modulating hypothalamopituitary functions, e.g., by altering the secretory pattern of GH. On the other hand, it seems that changes in the hypothalamopituitary functions are less significant for the inhibitory effect of estradiol on body growth. It is concluded from this study that the sites of action for estrogen and testosterone in modulating body growth in the rat are different.

Antidepressants do not modulate estrogen receptor α-mediated gene expression

2001 ◽  
Vol 108 (10) ◽  
pp. 1197-1202 ◽  
Author(s):  
B. Hermann ◽  
I. Vollmer ◽  
F. Holsboer ◽  
R. Rupprecht
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Estrogen Receptor Α

Selected Contribution: Estrogen receptor-α antisense decreases brain estrogen receptor levels and affects ventilation in male and female rats

2001 ◽  
Vol 91 (4) ◽  
pp. 1886-1892 ◽  
Author(s):  
Shashita R. Inamdar ◽  
Kathleen M. Eyster ◽  
Evelyn H. Schlenker
Keyword(s):  
Estrogen Receptor ◽  
Aspartic Acid ◽  
Estrogen Receptor Α ◽  
Neonatal Rat ◽  
Female Rats ◽  
Antisense Oligodeoxynucleotide ◽  
Protein Levels ◽  
Ventilatory Responses ◽  
Rat Pups ◽  
Male And Female Rats

We hypothesized that administration of an antisense oligodeoxynucleotide (ODN) to estrogen receptor (ER)-α mRNA decreases the ER protein in the neonatal rat brain, alters the sex-specific ventilatory responses to aspartic acid in rats, and counteracts the effects of testosterone proportionate (TP) in females. One-day-old rat pups were injected intraventricularly with vehicle, antisense ER ODN, or scrambled ODN control. Additional groups of females received TP or vehicle and one of the three treatments. Brain ER protein levels were decreased by 65% at 6 h and 35% at 24 h after antisense ODN. Aspartic acid decreased ventilation in all groups of weanling males and females except ER ODN-treated females and TP-vehicle-treated females. Aspartic acid decreased ventilation in all groups of adult females except those given TP and in males. Weanling ER ODN-treated rats were shorter and weighed less than controls. Only adult ER ODN-treated males exhibited these traits. Thus neonatal ER affects aspartic acid modulation of breathing and body growth in a sex-specific and developmental manner.

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