Postnatal Expression Patterns of Estrogen Receptor Subtypes and Choline Acetyltransferase in Different Regions of the Papez Circuit

2019 ◽  
Vol 41 (3-4) ◽  
pp. 203-211 ◽  
Author(s):  
Yu-xiang Wang ◽  
Lin Zhu ◽  
Li-xia Li ◽  
Hui-nan Xu ◽  
Hong-gang Wang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Choline Acetyltransferase ◽  
Brain Area ◽  
Expression Patterns ◽  
Female Rats ◽  
Long Term Memory ◽  
Receptor Subtypes ◽  
Brain Functions ◽  
Papez Circuit ◽  
G Protein Coupled

The Papez circuit is crucial for several brain functions, including long-term memory and emotion. Estradiol modulates cognitive functions based on the expression pattern of its receptor subtypes including estrogen receptor (ER) α, β, and G protein-coupled receptor 30 (GPR30). Similarly, the activity in the cholinergic system correlates with several brain functions, such as learning and memory. In this study, we used immunofluorescence to examine the expression patterns of ERβ and Western blotting to analyze GPR30 and choline acetyltransferase (ChAT) expression, in different regions of the Papez circuit, including the prefrontal cortex, hippocampus, hypothalamus, anterior nucleus of the thalamus, and cingulum in female rats at postnatal days (PND) 1, 10, and 56. Our main finding was that the highest expression of ERβ and GPR30 was noted in each brain area of the Papez circuit in the PND1 rats, whereas the expression of ChAT was the highest in PND10 rats. These results provide vital information on the postnatal expression patterns of ER subtypes and ChAT in different regions of the Papez circuit.

scholarly journals Estradiol activates epithelial sodium channels in rat alveolar cells through the G protein-coupled estrogen receptor

2013 ◽  
Vol 305 (11) ◽  
pp. L878-L889 ◽  
Author(s):  
Megan M. Greenlee ◽  
Jeremiah D. Mitzelfelt ◽  
Ling Yu ◽  
Qiang Yue ◽  
Billie Jeanne Duke ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Plasma Membrane ◽  
G Protein ◽  
Sodium Channels ◽  
Female Rats ◽  
Channel Activity ◽  
Alveolar Cells ◽  
Α Subunit ◽  
Female Sex ◽  
G Protein Coupled

Female sex predisposes individuals to poorer outcomes during respiratory disorders like cystic fibrosis and influenza-associated pneumonia. A common link between these disorders is dysregulation of alveolar fluid clearance via disruption of epithelial sodium channel (ENaC) activity. Recent evidence suggests that female sex hormones directly regulate expression and activity of alveolar ENaC. In our study, we identified the mechanism by which estradiol (E2) or progesterone (P4) independently regulates alveolar ENaC. Using cell-attached patch clamp, we measured ENaC single-channel activity in a rat alveolar cell line (L2) in response to overnight exposure to either E2 or P4. In contrast to P4, E2 increased ENaC channel activity ( NPo) through an increase in channel open probability ( Po) and an increased number of patches with observable channel activity. Apical plasma membrane abundance of the ENaC α-subunit (αENaC) more than doubled in response to E2 as determined by cell surface biotinylation. αENaC membrane abundance was approximately threefold greater in lungs from female rats in proestrus, when serum E2 is greatest, compared with diestrus, when it is lowest. Our results also revealed a significant role for the G protein-coupled estrogen receptor (Gper) to mediate E2's effects on ENaC. Overall, our results demonstrate that E2 signaling through Gper selectively activates alveolar ENaC through an effect on channel gating and channel density, the latter via greater trafficking of channels to the plasma membrane. The results presented herein implicate E2-mediated regulation of alveolar sodium channels in the sex differences observed in the pathogenesis of several pulmonary diseases.

scholarly journals Estrogen Receptor β: An Overview and Update

2008 ◽  
Vol 6 (1) ◽  
pp. nrs.06003 ◽  
Author(s):  
Chunyan Zhao ◽  
Karin Dahlman-Wright ◽  
Jan-Åke Gustafsson
Keyword(s):  
Estrogen Receptor ◽  
Target Genes ◽  
Expression Patterns ◽  
Estrogen Signaling ◽  
Receptor Subtypes ◽  
Specific Expression ◽  
Microarray Experiments ◽  
Downstream Target ◽  
Animal Disease Models ◽  
Selective Ligands

The discovery of a second estrogen receptor (ER), designated ERβ (NR3A2), has redefined our knowledge about the mechanisms underlying cellular signaling by estrogens and has broad implications for our understanding of regulation of estrogen-responsive tissues. Highly variable and even contrasting effects of estrogens in different tissues seem to be at least partially explained by different estrogen signaling pathways, involving ERα (NR3A1) and/or ERβ. To date, two key conclusions can be drawn from the significant body of work carried out on the specific roles of the two receptor subtypes in diverse estrogen target tissues. First, ERα and ERβ have different biological functions, as indicated by their specific expression patterns and the distinct phenotypes observed in ERα and ERβ knockout (αERKO and βERKO) mice. Second, ERα and ERβ appear to have overlapping but also unique sets of downstream target genes, as judged from a set of microarray experiments. Thus, ERα and ERβ have different transcriptional activities in certain ligand, cell-type, and promoter contexts, which may help to explain some of the major differences in their tissue-specific biological actions. The phenotypes observed for βERKO mice have suggested certain therapeutic areas to be further explored. The development of ERβ-selective ligands active in animal disease models indicates new avenues for clinical exploration. ERβ agonists are being explored and validated as drugs for a growing number of indications. Hopefully, some ERβ targeted drugs will prove to be efficient in enhancing human health.

scholarly journals Activation of G Protein-Coupled Estrogen Receptor 1 Ameliorates Proximal Tubular Injury and Proteinuria in Dahl Salt-Sensitive Female Rats

2021 ◽  
Author(s):  
Eman Y Gohar ◽  
Rawan N Almutlaq ◽  
Elizabeth M. Daugherty ◽  
Maryam K. Butt ◽  
Chunhua Jin ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Estrogen Receptor ◽  
Proximal Tubule ◽  
G Protein ◽  
Brush Border ◽  
Kidney Injury ◽  
Female Rats ◽  
Independent Manner ◽  
G Protein Coupled ◽  
Estrogen Receptor 1

Recent evidence indicates a crucial role for G protein-coupled estrogen receptor 1 (GPER1) in the maintenance of cardiovascular and kidney health in females. The current study tested whether GPER1 activation ameliorates hypertension and kidney damage in female Dahl salt-sensitive (SS) rats fed a high-salt (HS) diet. Adult female rats were implanted with telemetry transmitters for monitoring blood pressure and osmotic minipumps releasing G1 (selective GPER1 agonist, 400 μg/kg/day, intraperitoneal) or vehicle. Two weeks after pump implantation, rats were shifted from a normal salt diet (NS, 0.4% NaCl) to a matched HS diet (4.0% NaCl) for 2 weeks. 24-hour urine samples were collected during both diet periods and urinary markers of kidney injury were assessed. Histological assessment of kidney injury was conducted after the 2-week HS diet period. Compared with values during the NS diet, 24-hour mean arterial pressure markedly increased in response to HS, reaching similar values in vehicle-treated and G1-treated rats. HS also significantly increased urinary excretion of protein, albumin, nephrin (podocyte damage marker) and KIM-1 (proximal tubule injury marker) in vehicle-treated rats. Importantly, G1 treatment prevented the HS-induced proteinuria, albuminuria and increase in KIM-1 excretion but not nephrinuria. Histological analysis revealed that HS-induced glomerular damage did not differ between groups. However, G1 treatment preserved proximal tubule brush border integrity in HS-fed rats. Collectively, our data suggest that GPER1 activation protects against HS-induced proteinuria and albuminuria in female Dahl SS rats by preserving proximal tubule brush border integrity in a blood pressure-independent manner.

Abstract 041: New Evidence for G Protein-coupled Estrogen Receptor as a Natriuretic Factor

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Eman Y Gohar ◽  
Ijeoma E Obi ◽  
Carmen De Miguel ◽  
Jennifer S Pollock ◽  
David M Pollock
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
Sodium Excretion ◽  
Renal Medulla ◽  
Female Rats ◽  
Dietary Salt ◽  
Sd Rats ◽  
Urinary Potassium ◽  
G Protein Coupled ◽  
Sodium Handling

Premenopausal women have a lower risk of cardiovascular and renal diseases compared to age-matched men. This protection includes fewer salt-dependent complications. We have shown that female rats have a more robust natriuretic capacity compared to males in response to increased dietary salt. The novel estrogen receptor, G protein-coupled estrogen receptor (GPER), is a membrane-bound receptor linked to acute signaling pathways. GPER activation elicits protective effects throughout the cardiovascular system. However, its role in sodium handling is not defined. We hypothesized that activation of GPER in the renal medulla stimulates sodium excretion. In female Sprague Dawley (SD) rats, isosmotic saline was infused into the renal medullary interstitium (500 μl/h) during a 60-80 min equilibration period and 20 min baseline urine collection period. This was followed by infusion of the GPER agonist G1 (50 pmol/kg/min) or vehicle into the renal medulla for two further 20 min periods. Compared with vehicle, G1 significantly increased urinary sodium excretion and urine flow (from 0.5 ± 0.1 to 0.9 ± 0.2 μmol/min and from 5.3±1.1 to 8.3±1.6 μl/min, respectively, n=6, p<0.05). Urinary potassium excretion and mean arterial pressure remained unchanged during the experiments (0.5 ± 0.1 vs. 0.4 ± 0.1 μmol/min and 108.6 ± 3.4 vs. 107.2 ± 5.1 mmHg, respectively, n=6). Immunohistochemical analysis of GPER revealed more predominant staining in both inner and outer renal medulla in female SD rats, compared to males. GPER appears to be predominantly expressed in interstitial cells. These data reveal that renal medullary GPER plays an important role in renal sodium handling and may account for the enhanced ability to handle increased dietary salt in females. Funded by AHA 15POST25090329 to EYG and P01 HL136267 to DMP

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