Evidence map›Paper›PMID 23401547›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2013

Inhibition of the prostaglandin receptor EP2 following status epilepticus reduces delayed mortality and brain inflammation.

Jianxiong Jiang, Yi Quan, Thota Ganesh, Wendy A Pouliot, F Edward Dudek, Raymond Dingledine

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

111 citing papers in PubMed, 163 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Neuroinflammation and Disease: Pathways and Opportunities.Annual review of pharmacology and toxicology · 2026
    Review
  7. Targeting prostaglandin ENature communications · 2025
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

51 more citing papers are in PubMed but not listed here.

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

6 authors at 2 institutions in 1 country.

Jianxiong JiangDepartment of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA. jjiang3@emory.edu
Yi Quan
Thota Ganesh
Wendy A Pouliot
F Edward Dudek
Raymond Dingledine
Emory University · USUniversity of Utah · US

Funding

Prostanoid modulators that reduce brain injury and inflammation after seizuresU01NS058158 · NINDS · EMORY UNIVERSITY · PI DINGLEDINE, RAYMOND J · 2006 to 2015
$5.9M
Role of COX2 of Neuronal Origin in Blood-Brain Communication after status epileptR21NS074169 · NINDS · EMORY UNIVERSITY · PI DINGLEDINE, RAYMOND J · 2011 to 2012
$426k
Natural History and Treatment Response of AVMsK08NS042359 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI HALIM, ALEXANDER · 2002 to 2002
$131k
NINDS NIH HHS N01 NS042359NINDS NIH HHS R21 NS074169NINDS NIH HHS R21NS074169NINDS NIH HHS U01 NS058158NINDS NIH HHS U01NS058158
6 · The paper itself

Abstract

Prostaglandin E2 is now widely recognized to play critical roles in brain inflammation and injury, although the responsible prostaglandin receptors have not been fully identified. We developed a potent and selective antagonist for the prostaglandin E2 receptor subtype EP2, TG6-10-1, with a sufficient pharmacokinetic profile to be used in vivo. We found that in the mouse pilocarpine model of status epilepticus (SE), systemic administration of TG6-10-1 completely recapitulates the effects of conditional ablation of cyclooxygenase-2 from principal forebrain neurons, namely reduced delayed mortality, accelerated recovery from weight loss, reduced brain inflammation, prevention of blood-brain barrier opening, and neuroprotection in the hippocampus, without modifying seizures acutely. Prolonged SE in humans causes high mortality and morbidity that are associated with brain inflammation and injury, but currently the only effective treatment is to stop the seizures quickly enough with anticonvulsants to prevent brain damage. Our results suggest that the prostaglandin receptor EP2 is critically involved in neuroinflammation and neurodegeneration, and point to EP2 receptor antagonism as an adjunctive therapeutic strategy to treat SE.

Indexed as

AnimalsAnticonvulsantsBlood-Brain BarrierBrainDisease Models, AnimalHippocampusHumansIndolesInflammationMiceModels, NeurologicalNerve DegenerationPilocarpineReceptors, Prostaglandin E, EP2 SubtypeRecovery of FunctionStatus EpilepticusAnticonvulsantsIndolesPilocarpineReceptors, Prostaglandin E, EP2 Subtype

Identifiers

PMID23401547
PMCPMC3587237
OpenAlexW1974631216

What OpenQuestion holds

Textmetadata
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.