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g protein-coupled estrogen receptor 1 Negatively Regulates the Proliferation of Mouse-Derived Neural Stem/Progenitor Cells via Extracellular Signal-regulated Kinase Pathway

G Protein-Coupled Estrogen Receptor 1 Negatively Regulates t...

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第十四届中国医师协会神经外科医师年会

作者： Jun Zhong Hong-fei ge Chao Zhang Jing-yu Chen Huan-huan Li Xuan-yu Fang Liang Tan Xin Liu Zheng-cai Jia Hua Feng Rong Hu Department of Neurosurgery and Key Laboratory of Neurotrauma Southwest HospitalThird Military Medical University （Army Medical university）

g protein-coupled estrogen receptor 1（gPER1, also known as gPR30） has been reported to play a wide range of function in the central nervous system（CNS）. However, whether gPER1 is expressed by neural stem/progenitor cells（NSPCs） and its role has not been established. Here, we found the expression of gPER1 in mouse-derived NSPCs via western blot and immunofluorescent staining. Moreover, we revealed that specific activation of gPER1 by the agonist g1 decreased the proliferation of NSPCs in a dose-dependent manner. The neurosphere formation assay and Ki67 staining further demonstrated that activation of gPER1 inhibited the proliferation of NSPCs. Additionally, the inhibitory effect of g1 on the proliferation of NSPCs could be blocked by the specific gPER1 antagonist g15. Intriguingly, ERK pathway was involved in the negative effect of gPER1 on the proliferation of NSPCs, because the phosphorylation level of ERK in NSPCs was remarkably decreased during g1 treatment. However, the antagonist g15 reversed the down-regulated level of p-ERK. Knock-down gPER1 also reversed the inhibitory effect of g1 on NSPCs proliferation. Together, our results provide the first evidence that gPER1 is expressed by NSPCs and its activation negatively modulates the proliferation of NSPCs, highlighting the importance of gPER1 in regulating NSPC behaviors.

关键词： Neural stem/progenitor cells g protein-coupled estrogen receptor 1 Proliferation Extracellular signal-regulated kinase

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Molecular mechanism of endocrine-disruptive effects induced by Bisphenol A:The role of transmembrane g-protein estrogen receptor 1 and integrin αvβ3

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Journal of Environmental Sciences 2019年第1期31卷 1-13页

作者： Zhiguo Sheng Cong Wang Furong Ren Yuxiang Liu Benzhan Zhu Research Center for Eco-Environmental Sciences Chinese Academy of Sciences University of Chinese Academy of Sciences College of Chemistry and Chemical Engineering Xinjiang Normal University

Bisphenol A(BPA) is one of the highest volume industrial products worldwide and has been widely used to make various products as the intermediates of polycarbonate plastics and epoxy ***, general population has been widely exposed to BPA due to extensive use of BPAcontaining products. BPA has similar chemical structure with the natural estrogen and has been shown to induce a variety of estrogen-like endocrine effects on organism in vivo or in vitro. High doses of BPA tend to act as antagonist of estrogen receptors(ERs) by directly regulating the genomic transcription. However, BPA at environmentally relevant low-dose always disrupt the biological function via a non-genomic manner mediated by membrane receptors, rather than ERs. Although some studies had investigated the non-genomic effects of low-dose BPA, the exact molecular mechanism still remains unclear. Recently, we found that membrane g protein-coupled estrogen receptor 1 and integrin αvβ3 and its relative signal pathways participate in the induction of male germ cell proliferation and thyroid transcription disruption by the low-dose BPA. A profound understanding for the mechanism of action of the environmentally relevant BPA exposure not only contributes to objectively evaluate and predict the potential influence to human health, but also provides theoretical basis and methodological support for assessing health effects trigged by other estrogen-like environmental endocrine disruptors. Based mainly on our recent findings, this review outlines the research progress of molecular mechanism on endocrine disrupting effects of environmental low-dose BPA, existing problems and some consideration for future studies.

关键词： Bisphenol A Low-dose effects g protein-coupled estrogen receptor 1 Integrin αvβ3 Reproductive toxicity Thyroxine interference effect

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