Tricresyl phosphate isomers exert estrogenic effects via G protein-coupled estrogen receptor-mediated pathways

2020 ◽  
Vol 264 ◽  
pp. 114747
Author(s):  
Xiaoya Ji ◽  
Na Li ◽  
Mei Ma ◽  
Kaifeng Rao ◽  
Rong Yang ◽  
...  
2014 ◽  
Vol 22 (1) ◽  
pp. 87-98 ◽  
Author(s):  
Wanglong Zhang ◽  
Yu Luo ◽  
Li Zhang ◽  
Qian Cai ◽  
Xuejun Pan

A variety of endocrine-disrupting chemicals (EDCs) have estrogenic effects and are termed xenoestrogens (XEs). The genomic pathway mediated by estrogen receptors (ERs) has been considered the major explanation for the estrogenic effects elicited by XEs. Presently, nongenomic pathways have achieved considerably more attention because the genomic pathways cannot fully elucidate many biological and physiological responses. Genomic and nongenomic pathways act either separately or cooperatively. XEs activate a variety of signaling pathways and downstream kinases, which in turn alter the posttranslational modification and activation of ERs. Classical ERs and their splice variants reside at the membrane and mediate rapid effects cooperatively with G protein-coupled estrogen receptor 1 (GPER), G protein, and many other signaling molecules. GPER seems more effective in mediating the synthetic chemical-induced effects. There are also feedback and feedforward mechanisms between both pathways. Numerous factors may affect both pathways. Recently, some new layers of regulation on the estrogenic effects were identified. In this review, we summarize these multiple regulation layers and discuss the newly identified factors.


2017 ◽  
Vol 51 (19) ◽  
pp. 11423-11430 ◽  
Author(s):  
Lin-Ying Cao ◽  
Xiao-Min Ren ◽  
Chuan-Hai Li ◽  
Jing Zhang ◽  
Wei-Ping Qin ◽  
...  

2018 ◽  
Vol 126 (5) ◽  
pp. 057005 ◽  
Author(s):  
Lin-Ying Cao ◽  
Xiao-Min Ren ◽  
Yu Yang ◽  
Bin Wan ◽  
Liang-Hong Guo ◽  
...  

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Danielle S Macêdo ◽  
Lia Lira Olivier Sanders ◽  
Raimunda das Candeias ◽  
Cyntia de Freitas Montenegro ◽  
David Freitas de Lucena ◽  
...  

Abstract The observation that a person’s sex influences the onset age of schizophrenia, the course of the disease, and antipsychotic treatment response suggests a possible role for estrogen receptors in the pathophysiology of schizophrenia. Indeed, treatment with adjunctive estrogen or selective estrogen receptor modulators (SERMs) are known to reduce schizophrenia symptoms. While estrogen receptors (ER)α and ERβ have been studied, a third and more recently discovered estrogen receptor, the G protein-coupled estrogen receptor 1 (GPER), has been largely neglected. GPER is a membrane receptor that regulates non-genomic estrogen functions, such as the modulation of emotion and inflammatory response. This review discusses the possible role of GPER in brain impairments seen in schizophrenia and in its potential as a therapeutic target. We conducted a comprehensive literature search in the PubMed/MEDLINE database, using the following search terms: “Schizophrenia,” “Psychosis,” “GPER1 protein,” “Estrogen receptors,” “SERMS,” “GPER1 agonism, “Behavioral symptoms,” “Brain Inflammation.” Studies involving GPER in schizophrenia, whether preclinical or human studies, have been scarce, but the results are encouraging. Agonism of the GPER receptor could prove to be an essential mechanism of action for a new class of “anti-schizophrenia” drugs.


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