ArticleBioscience reports2016
G-1 exerts neuroprotective effects through G protein-coupled estrogen receptor 1 following spinal cord injury in mice.
Article in Bioscience reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- The role of sex hormones in neurological and functional recovery following spinal cord injury in females: a systematic review of the literature.Spinal cord · 2026Pooled it
- Neuroprotective effects of baicalin and baicalein on the central nervous system and the underlying mechanisms.Heliyon · 2025Review
- Hormonal regulatory networks in spinal cord injury: mechanistic insights, crosstalk, and therapeutic innovations.Frontiers in endocrinology · 2025Review
- Advances of the MAPK pathway in the treatment of spinal cord injury.CNS neuroscience & therapeutics · 2024Review
- Involvement of the G-Protein-Coupled Estrogen Receptor-1 (GPER) Signaling Pathway in Neurodegenerative Disorders: A Review.Cellular and molecular neurobiology · 2023Review
- Baicalin attenuates blood-spinal cord barrier disruption and apoptosis through PI3K/Akt signaling pathway after spinal cord injury.Neural regeneration research · 2022Article
- Shikonin Mediates Apoptosis through G Protein-Coupled Estrogen Receptor of Ovarian Cancer Cells.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- The chronification mechanism of orofacial inflammatory pain: Facilitation by GPER1 and microglia in the rostral ventral medulla.Frontiers in molecular neuroscience · 2022Article
- Urolithin A as a Potential Drug for the Treatment of Spinal Cord Injuries: A Mechanistic Study Using Network Pharmacology Approaches.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- From Menopause to Neurodegeneration-Molecular Basis and Potential Therapy.International journal of molecular sciences · 2021Review
- G protein-coupled estrogen receptor 1 (GPER) activation triggers different signaling pathways on neurons and astrocytes.Neural regeneration research · 2019Article
- GPR30-mediated estrogenic regulation of actin polymerization and spatial memory involves SRC-1 and PI3K-mTORC2 in the hippocampus of female mice.CNS neuroscience & therapeutics · 2019Article
- Icariin Inhibits Endoplasmic Reticulum Stress-induced Neuronal Apoptosis after Spinal Cord Injury through Modulating the PI3K/AKT Signaling Pathway.International journal of biological sciences · 2019Article
- The novel estrogenic receptor GPR30 alleviates ischemic injury by inhibiting TLR4-mediated microglial inflammation.Journal of neuroinflammation · 2018Article
- MiR-25 protects PC-12 cells from HThe journal of spinal cord medicine · 2018Article
- GPER modulators: Opportunity Nox on the heels of a class Akt.The Journal of steroid biochemistry and molecular biology · 2018Review
- Continuous tamoxifen delivery improves locomotor recovery 6h after spinal cord injury by neuronal and glial mechanisms in male rats.Experimental neurology · 2018Article
- Hormonal therapy in traumatic spinal cord injury.American journal of translational research · 2017Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) always occurs accidently and leads to motor dysfunction because of biochemical and pathological events. Estrogen has been shown to be neuroprotective against SCI through estrogen receptors (ERs), but the underlying mechanisms have not been fully elucidated. In the present study, we investigated the role of a newly found membrane ER, G protein-coupled estrogen receptor 1 (GPR30 or GPER1), and discussed the feasibility of a GPR30 agonist as an estrogen replacement. Forty adult female C57BL/6J mice (10-12 weeks old) were divided randomly into vehicle, G-1, E2, G-1 + G-15 and E2 + G-15 groups. All mice were subjected to SCI using a crushing injury approach. The specific GPR30 agonist, G-1, mimicked the effects of E2 treatment by preventing SCI-induced apoptotic cell death and enhancing motor functional recovery after injury. GPR30 activation regulated phosphatidylinositol 3-kinase (PI3K)/Akt and MAPK/extracellular signal-regulated kinase (ERK) signalling pathways, increased GPR30 and anti-apoptosis proteins Bcl-2 and brain derived neurotrophic factor (BDNF), but decreased the pro-apoptosis factor Bax and cleaved caspase-3. However, the neuroprotective effects of G-1 and E2 were blocked by the specific GPR30 antagonist, G-15. Thus, GPR30 rather than classic ERs is required to induce estrogenic neuroprotective effects. Given that estrogen replacement therapy may cause unexpected side effects, especially on the reproductive system, GPR30 agonists may represent a potential therapeutic approach for treating SCI.
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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.