Evidence map›Paper›PMID 25872489›Full record

ArticleMolecular medicine reports2015

G-protein-coupled receptor 30-mediated antiapoptotic effect of estrogen on spinal motor neurons following injury and its underlying mechanisms.

Jingyu Chen, Rong Hu, Hongfei Ge, Wangsheng Duanmu, Yuhong Li, Xingseng Xue, Shengli Hu, Hua Feng

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

16 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Hormonal therapy in traumatic spinal cord injury.American journal of translational research · 2017
    Review
  15. Article
  16. Review
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 2 institutions in 1 country.

Jingyu ChenDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Rong HuDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Hongfei GeDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Wangsheng DuanmuDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Yuhong LiDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Xingseng XueDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Shengli HuDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Hua FengDepartment of Neurosurgery, Southwest Hospital, Third Military Medical University, Chongqing 400038, P.R. China.
Southwest Hospital · CNArmy Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spinal cord injury (SCI) may result in severe dysfunction of motor neurons. G-protein-coupled receptor 30 (GPR30) expression in the motor neurons of the ventral horn of the spinal cord mediates neuroprotection through estrogen signaling. The present study explored the antiapoptotic effect of estrogen, mediated by GPR30 following SCI, and the mechanisms underlying this effect. Spinal motor neurons from rats were cultured in vitro in order to establish cell models of oxygen and glucose deprivation (OGD). The effects of estrogen, the estrogen agonist, G1, and the estrogen inhibitor, G15, on motor neurons were observed using MTT assays. The effects of E2, G1 and G15 on spinal motor neuron apoptosis following OGD, were detected using flow cytometry. The role of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) inhibitor, LY294002, was also determined using flow cytometry. Rat SCI models were established. E2, G1 and E2+LY294002 were administered in vivo. Motor function was scored at 3, 7, 14, 21 and 28 d following injury, using Basso-Beattie-Bresnahan (BBB) standards. Cell activity in the estrogen and G1 groups was higher than that in the solvent group, whereas cell activity in the E2+G15 group was lower than that in the E2 group (P<0.05). Following OGD, the proportion of apoptotic cells significantly increased (P<0.05). The proportion in the estrogen group was significantly lower than that in the solvent group, whereas the proportion of apoptotic cells in the E2+G15 and E2+LY294002 groups was higher than that in the E2 group (P<0.05). Treatment with E2 and G1 led to upregulation of P-Akt expression in normal cells and post-OGD cells. The BBB scores of rats in the E2 and G1 groups were higher than those in the placebo group (P<0.05). The BBB scores of the E2+LY294002 group were lower than those of the E2 group (P<0.05). Estrogen thus appears to exert a protective effect on spinal motor neurons following OGD, via GPR30. The PI3K/Akt pathway may be one of those involved in the estrogen‑related antiapoptotic effects mediated by GPR30.

Indexed as

AnimalsApoptosisCells, CulturedChromonesEstradiolMaleMicroscopy, FluorescenceModels, BiologicalMorpholinesMotor NeuronsPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPhosphorylationProto-Oncogene Proteins c-aktRatsRats, Sprague-Dawley2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneChromonesEstradiolGper1 protein, ratMorpholinesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktReceptors, G-Protein-Coupled

Identifiers

PMID25872489
PMCPMC4464192
OpenAlexW2002656992

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.