Evidence map›Paper›PMID 21939736›Full record

ArticleNeuroscience letters2011

Function of prostaglandin E2 EP receptors in the acute outcome of rodent hypoxic ischemic encephalopathy.

Hidetoshi Taniguchi, Christoph Anacker, Gabriela Beatriz Suarez-Mier, Qian Wang, Katrin Andreasson

Abstract read
In one paragraph

Article in Neuroscience letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  6. Anti-Inflammatory and Neuroprotective Effects of PGEJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2017
    Article
  7. Cerebroprotection by the neuronal PGE2 receptor EP2 after intracerebral hemorrhage in middle-aged mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  8. Review
  9. Article
  10. Article
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  14. Review
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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

5 authors at 1 institution in 1 country.

Hidetoshi TaniguchiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA. hide-tan@ped.med.osaka-u.ac.jp
Christoph Anacker
Gabriela Beatriz Suarez-Mier
Qian Wang
Katrin Andreasson
Stanford University · US

Funding

Protective Prostaglandin Receptors in Cerebral IschemiaR01NS045727 · NINDS · STANFORD UNIVERSITY · PI ANDREASSON, KATRIN I. · 2004 to 2015
$3.7M
NINDS NIH HHS R01 NS045727NINDS NIH HHS R01NS045727
6 · The paper itself

Abstract

Neonatal hypoxic-ischemic encephalopathy (HIE) is a leading cause of severe and permanent neurologic disability after birth. The inducible cyclooxygenase COX-2, which along with COX-1 catalyzes the first committed step in prostaglandin (PG) synthesis, elicits significant brain injury in models of cerebral ischemia; however its downstream PG receptor pathways trigger both toxic and paradoxically protective effects. Here, we investigated the function of PGE(2) E-prostanoid (EP) receptors in the acute outcome of hypoxic-ischemic (HI) injury in the neonatal rat. We determined the temporal and cellular expression patterns of the EP1-4 receptors before and after HIE and tested whether modulation of EP1-4 receptor function could protect against cerebral injury acutely after HIE. All four EP receptors were expressed in forebrain neurons and were induced in endothelial cells after HIE. Inhibition of EP1 signaling with the selective antagonist SC-51089 or co-activation of EP2-4 receptors with the agonist misoprostol significantly reduced HIE cerebral injury 24 h after injury. These receptor ligands also protected brain endothelial cells subjected to oxygen glucose deprivation, suggesting that activation of EP receptor signaling is directly cytoprotective. These data indicate that the G-protein coupled EP receptors may be amenable to pharmacologic targeting in the acute setting of neonatal HIE.

Indexed as

AnimalsAnimals, NewbornCells, CulturedDinoprostoneEndothelial CellsGlucoseHippocampusHydrazinesHypoxia-Ischemia, BrainMisoprostolNeuronsOxazepinesOxygenRatsRats, Sprague-DawleyReceptors, Prostaglandin E, EP1 SubtypeDinoprostoneGlucoseHydrazinesMisoprostolOxazepinesOxygenReceptors, Prostaglandin E, EP1 SubtypeReceptors, Prostaglandin E, EP2 SubtypeReceptors, Prostaglandin E, EP3 SubtypeReceptors, Prostaglandin E, EP4 SubtypeSC 51089

Identifiers

PMID21939736
PMCPMC3210938
OpenAlexW2049561958

What OpenQuestion holds

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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.