Evidence map›Paper›PMID 29484405›Full record

ArticleMolecular medicine reports2018

Downregulation of G‑protein‑coupled receptor 30 in the hippocampus attenuates the neuroprotection of estrogen in the critical period hypothesis.

Yingxi Wu, Dayun Feng, Jiaji Lin, Yan Qu, Shiming He, Yuan Wang, Guodong Gao, Tianzhi Zhao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 19% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 14 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Yingxi Wu *Department of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Dayun Feng *Department of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Jiaji Lin *Department of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Yan QuDepartment of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Shiming HeDepartment of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Yuan WangDepartment of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Guodong GaoDepartment of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Tianzhi ZhaoDepartment of Neurosurgery, Tangdu Hospital of The Fourth Military Medical University, Xi'an, Shaanxi 710038, P.R. China.
Air Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the role of G‑protein‑coupled receptor 30 (GPR30) in long‑term 17β‑estradiol (E2) deprivation (LTED) in a rat model with global cerebral ischemia (GCI), and its therapeutic target for ischemic stroke in the clinical setting. Following bilateral ovariectomy, GCI was induced in rats 1 or 10 weeks post‑surgery. To determine the protein and mRNA expression levels of GPR30 in the hippocampal CA1 region of LTED rats, short‑term E2 deprivation (STED) rats and naturally aging rats, western blot analysis and reverse transcription-quantitative polymerase chain reaction were performed. The results of the present study demonstrated that E2 treatment revealed significant neuroprotection post‑GCI in STED rats, but not in LTED rats, as well as a decrease in the expression levels of GPR30 in the hippocampal CA1 region. In LTED rats,. Notably, no effects were observed on the ubiquitination of GPR30 following investigation in STED or LTED rats. While the protein and mRNA expression levels of GPR30 were also decreased in the hippocampal CA1 region of female 24‑month‑old rats compared with 3‑month‑old rats. E2 treatment initiated for the entire ovariectomy period elevated GPR30 mRNA and protein expression levels, and attenuated the loss of hippocampal neurons in the GCI‑induced CA1 region, indicating that E2 treatment exerted robust neuroprotection within LTED rats. However, the neuroprotective effect of E2 may be blocked by G15. The results of the present study revealed that downregulation of GPR30 expression may attenuate the neuroprotection of E2 within LTED conditions in rats post‑ovariectomy by leading to neuronal insensitivity to E2 neuroprotection following cerebral ischemia. These results provide evidence that GPR30 may have potential as a novel therapeutic target for the treatment of clinical ischemic stroke.

Indexed as

NeuroprotectionAge FactorsAnimalsBrain IschemiaCA1 Region, HippocampalCell SurvivalEstrogensFemaleFluorescent Antibody TechniqueGene Expression RegulationHippocampusOvariectomyPyramidal CellsRatsReceptors, G-Protein-CoupledRNA, MessengerEstrogensGper1 protein, ratReceptors, G-Protein-CoupledRNA, MessengerestradiolG15 antagonistG1 agonistG-protein-coupled receptor 30hippocampusneuroprotection

Identifiers

PMID29484405
PMCPMC5866014
OpenAlexW2792187438

What OpenQuestion holds

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Registered trials

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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.