ArticleThe Journal of biological chemistry2012
GPR30 regulates glutamate transporter GLT-1 expression in rat primary astrocytes.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 91 citations in OpenAlex.
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- Exploring the role of sex hormones and gender diversity in multiple sclerosis.Nature reviews. Neurology · 2025Article
- Astrocytic glutamate transport is essential for the memory-enhancing effects of 17β-estradiol in ovariectomized mice.Hormones and behavior · 2024Article
- PFOS Elicits Cytotoxicity in Neuron Through Astrocyte-Derived CaMKII-DLG1 Signaling In Vitro Rat Hippocampal Model.Neurochemical research · 2024Article
- Targeting Reactive Astrocytes in Vascular Dementia: Investigation of Neuronal-Astrocyte-Vascular Interactions.Neuroscience insights · 2024Article
- Article
- Structures and coordination chemistry of transporters involved in manganese and iron homeostasis.Biochemical Society transactions · 2023Review
- The effects of GPER on age-associated memory impairment induced by decreased estrogen levels.Frontiers in molecular biosciences · 2023Review
- High-fat diet induces depression-like phenotype via astrocyte-mediated hyperactivation of ventral hippocampal glutamatergic afferents to the nucleus accumbens.Molecular psychiatry · 2022Article
- Sex steroid hormone function in the brain niche: Implications for brain metastatic colonization and progression.Cancer reports (Hoboken, N.J.) · 2022Review
- The chronification mechanism of orofacial inflammatory pain: Facilitation by GPER1 and microglia in the rostral ventral medulla.Frontiers in molecular neuroscience · 2022Article
- Activation of p38 MAPK participates in the sulbactam-induced cerebral ischemic tolerance mediated by glial glutamate transporter-1 upregulation in rats.Scientific reports · 2020Article
- The Resurrection of Phenotypic Drug Discovery.ACS medicinal chemistry letters · 2020Article
- Estrogen and progesterone attenuate glutamate neurotoxicity via regulation of EAAT3 and GLT-1 in a rat model of ischemic stroke.Iranian journal of basic medical sciences · 2020Article
- It takes a neural village: Circuit-based approaches for estrogenic regulation of episodic memory.Frontiers in neuroendocrinology · 2020Review
- Estrogen Signaling in Alzheimer's Disease: Molecular Insights and Therapeutic Targets for Alzheimer's Dementia.Molecular neurobiology · 2020Review
- Microglial and Astrocytic Function in Physiological and Pathological Conditions: Estrogenic Modulation.International journal of molecular sciences · 2020Review
- The Role of Sex and Sex Hormones in Neurodegenerative Diseases.Endocrine reviews · 2020Review
- Effect of Combined Prenatal and Adult Benzophenone-3 Dermal Exposure on Factors Regulating Neurodegenerative Processes, Blood Hormone Levels, and Hematological Parameters in Female Rats.Neurotoxicity research · 2020Article
- The role of astrocytic glutamate transporters GLT-1 and GLAST in neurological disorders: Potential targets for neurotherapeutics.Neuropharmacology · 2019Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
The G protein-coupled estrogen receptor GPR30 contributes to the neuroprotective effects of 17β-estradiol (E2); however, the mechanisms associated with this protection have yet to be elucidated. Given that E2 increases astrocytic expression of glutamate transporter-1 (GLT-1), which would prevent excitotoxic-induced neuronal death, we proposed that GPR30 mediates E2 action on GLT-1 expression. To investigate this hypothesis, we examined the effects of G1, a selective agonist of GPR30, and GPR30 siRNA on astrocytic GLT-1 expression, as well as glutamate uptake in rat primary astrocytes, and explored potential signaling pathways linking GPR30 to GLT-1. G1 increased GLT-1 protein and mRNA levels, subject to regulation by both MAPK and PI3K signaling. Inhibition of TGF-α receptor suppressed the G1-induced increase in GLT-1 expression. Silencing GPR30 reduced the expression of both GLT-1 and TGF-α and abrogated the G1-induced increase in GLT-1 expression. Moreover, the G1-induced increase in GLT-1 protein expression was abolished by a protein kinase A inhibitor and an NF-κB inhibitor. G1 also enhanced cAMP response element-binding protein (CREB), as well as both NF-κB p50 and NF-κB p65 binding to the GLT-1 promoter. Finally, to model dysfunction of glutamate transporters, manganese was used, and G1 was found to attenuate manganese-induced impairment in GLT-1 protein expression and glutamate uptake. Taken together, the present data demonstrate that activation of GPR30 increases GLT-1 expression via multiple pathways, suggesting that GPR30 is worthwhile as a potential target to be explored for developing therapeutics of excitotoxic neuronal injury.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.