Marijuana and β-estradiol interactions on spatial learning and memory in young female rats: Lack of role of the G protein-coupled estrogen receptor (GPR30)

Life Sciences ◽  
2021 ◽  
pp. 119723
Author(s):  
Mohadeseh Chahkandi ◽  
Gholamreza Komeili ◽  
Gholamreza Sepehri ◽  
Mohammad Khaksari ◽  
Sedigheh Amiresmaili
Keyword(s):  
Estrogen Receptor ◽  
Learning And Memory ◽  
G Protein ◽  
Spatial Learning ◽  
Young Female ◽  
Female Rats ◽  
Spatial Learning And Memory ◽  
G Protein Coupled

The role of the central histaminergic receptors in the exercise-induced improvements of the spatial learning and memory in rats

2014 ◽  
Vol 1587 ◽  
pp. 112-118 ◽  
Author(s):  
Majid Taati ◽  
Mehrnoush Moghaddasi ◽  
Masoumeh Esmaeili ◽  
Soheila Pourkhodadad ◽  
Hassan Nayebzadeh
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Spatial Learning And Memory ◽  
Exercise Induced

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 Perspectives on the Role of Non-Coding RNAs in the Regulation of Expression and Function of the Estrogen Receptor

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2162
Author(s):  
Mohammad Taheri ◽  
Hamed Shoorei ◽  
Marcel E. Dinger ◽  
Soudeh Ghafouri-Fard
Keyword(s):  
Estrogen Receptor ◽  
G Protein ◽  
Reproductive System ◽  
Estrogen Regulation ◽  
Tissue Specific ◽  
Membrane Bound ◽  
Non Coding Rnas ◽  
And Function ◽  
G Protein Coupled

Estrogen receptors (ERs) comprise several nuclear and membrane-bound receptors with different tissue-specific functions. ERα and ERβ are two nuclear members of this family, whereas G protein-coupled estrogen receptor (GPER), ER-X, and Gq-coupled membrane estrogen receptor (Gq-mER) are membrane-bound G protein-coupled proteins. ERα participates in the development and function of several body organs such as the reproductive system, brain, heart and musculoskeletal systems. ERβ has a highly tissue-specific expression pattern, particularly in the female reproductive system, and exerts tumor-suppressive roles in some tissues. Recent studies have revealed functional links between both nuclear and membrane-bound ERs and non-coding RNAs. Several oncogenic lncRNAs and miRNAs have been shown to exert their effects through the modulation of the expression of ERs. Moreover, treatment with estradiol has been shown to alter the malignant behavior of cancer cells through functional axes composed of non-coding RNAs and ERs. The interaction between ERs and non-coding RNAs has functional relevance in several human pathologies associated with estrogen regulation, such as cancers, intervertebral disc degeneration, coronary heart disease and diabetes. In the current review, we summarize scientific literature on the role of miRNAs and lncRNAs on ER-associated signaling and related disorders.

scholarly journals G Protein-Coupled Estrogen Receptor 1 Regulates Human Neutrophil Functions

2017 ◽  
Vol 2 (1) ◽  
pp. 1-13 ◽  
Author(s):  
M. Carmen Rodenas ◽  
Nicola Tamassia ◽  
Isabel Cabas ◽  
Federica Calzetti ◽  
José Meseguer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Estrogen Receptor ◽  
Protein Kinase ◽  
G Protein ◽  
Respiratory Burst ◽  
Human Neutrophils ◽  
G Protein Coupled ◽  
Estrogen Receptor 1

Background: The role of estrogens in immune functioning is relatively well known under both physiological and pathological conditions. Neutrophils are the most abundant circulating leukocytes in humans, and their abundance and function are regulated by estrogens, since they express estrogen receptors (ERs). Traditionally, estrogens were thought to act via classical nuclear ERs, namely ERα and ERβ. However, it was observed that some estrogens induced biological effects only minutes after their application. This rapid, “nongenomic” effect of estrogens is mediated by a membrane-anchored receptor called G protein-coupled estrogen receptor 1 (GPER1). Nevertheless, the expression and role of GPER1 in the immune system has not been exhaustively studied, and its relevance in neutrophil functions remains unknown. Methods: Human neutrophils were incubated in vitro with 10-100 µM of the GPER1-specific agonist G1 alone or in combination with lipopolysaccharide. GPER1 expression and subcellular localization, respiratory burst, life span, gene expression profile, and cell signaling pathways involved were then analyzed in stimulated neutrophils. Results: Human neutrophils express a functional GPER1 which regulates their functions through cAMP/protein kinase A/cAMP response element-binding protein, p38 mitogen-activated protein kinase, and extracellular regulated MAPK signaling pathways. Thus, GPER1 activation in vitro increases the respiratory burst of neutrophils, extends their life span, and drastically alters their gene expression profile. Conclusions: Our results demonstrate that GPER1 activation promotes the polarization of human neutrophils towards a proinflammatory phenotype and point to GPER1 as a potential therapeutic target in immune diseases where neutrophils play a key role.

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