scholarly journals Stroke Increases G Protein-Coupled Estrogen Receptor Expression in the Brain of Male but Not Female Mice

Neurosignals ◽  
2013 ◽  
Vol 21 (3-4) ◽  
pp. 229-239 ◽  
Author(s):  
Brad R.S. Broughton ◽  
Vanessa H. Brait ◽  
Elizabeth Guida ◽  
Seyoung Lee ◽  
Thiruma V. Arumugam ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
Receptor Expression ◽  
Estrogen Receptor Expression ◽  
Female Mice ◽  
G Protein Coupled ◽  
The Brain

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.

scholarly journals Activation of Estrogen Receptor G Protein–Coupled Receptor 30 Enhances Cholesterol Cholelithogenesis in Female Mice

Hepatology ◽  
2020 ◽  
Vol 72 (6) ◽  
pp. 2077-2089 ◽  
Author(s):  
Helen H. Wang ◽  
Ornella Bari ◽  
Christopher K. Arnatt ◽  
Min Liu ◽  
Piero Portincasa ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
G Protein Coupled Receptor ◽  
Female Mice ◽  
G Protein Coupled

Impact of Aging and G Protein‐Coupled Estrogen Receptor Deletion in Arterial Stiffening and Cardiac Function in Male and Female Mice

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Benard Ojwang Ogola ◽  
Margaret A. Zimmerman ◽  
Nicholas R. Harris ◽  
Isabella Kilanowski-Doroh ◽  
Leanne Groban ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cardiac Function ◽  
G Protein ◽  
Male And Female ◽  
Arterial Stiffening ◽  
Female Mice ◽  
G Protein Coupled

scholarly journals G Protein‐Coupled Estrogen Receptor 1 is Required for Greater Endothelin‐1 Excretion in Female Mice

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Ginger Guthrie ◽  
Rawan Almutlaq ◽  
Maryam Butt ◽  
David Pollock ◽  
Eman Gohar
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
Female Mice ◽  
Endothelin 1 ◽  
G Protein Coupled ◽  
Estrogen Receptor 1

scholarly journals G Protein–Coupled Estrogen Receptor 30 Reduces Transverse Aortic Constriction–Induced Myocardial Fibrosis in Aged Female Mice by Inhibiting the ERK1/2 -MMP-9 Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Xiaowu Wang ◽  
Jipeng Ma ◽  
Shuaishuai Zhang ◽  
Zilin Li ◽  
Ziwei Hong ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Cardiovascular Diseases ◽  
G Protein ◽  
Myocardial Fibrosis ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction ◽  
Female Mice ◽  
G Protein Coupled ◽  
Tgf Β1

The incidence of cardiovascular diseases was significantly increased in postmenopausal women. The protection of estrogen in the cardiovascular system has been further reported for decades. Although menopausal hormone therapy has been used in many clinical trials, the debatable results indicate that the studies for elucidating the precise molecular mechanism are urgently required. G protein–coupled estrogen receptor 30 (GPR30) is a membrane receptor of estrogen and displays protective roles in diverse cardiovascular diseases. Previous studies have revealed that ERK1/2-mediated MMP-9 signaling was involved in ischemic heart diseases. However, the role of ERK1/2-mediated MMP-9 signaling in the protection of GPR30 against cardiac hypertrophy in aged female mice has not been investigated. Our present study demonstrated that GPR30 overexpression and its agonist G1 co-administration reduced transverse aortic constriction–induced myocardial fibrosis and preserved cardiac function in aged female mice. MMP-9 expression was markedly increased via ERK1/2 phosphorylation in transverse aortic constriction–injured myocardium of aged female mice. Further results showed that GPR30/G1 activation decreased MMP-9 expression via ERK1/2 inhibition, which further reduced TGF-β1 expression. Inhibition of the ERK1/2 signaling pathway by its inhibitor PD98059 suppressed the induction of the cardiomyocyte MMP-9 level caused by the GRP30 antagonist G15 and inhibited TGF-β1 expression in cardiac fibroblast in vitro. In summary, our results from in vivo and in vitro studies indicated that GPR30 activation inhibited myocardial fibrosis and preserved cardiac function via inhibiting ERK-mediated MMP-9 expression. Thus, the present study may provide the novel drug targets for prevention and treatment of cardiac pathological hypertrophy in postmenopausal women.

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