Evidence map›Paper›PMID 21376752›Full record

ReviewNeurotoxicology2011

Prostanoid signaling: dual role for prostaglandin E2 in neurotoxicity.

Dejan Milatovic, Thomas J Montine, Michael Aschner

Abstract readReview
In one paragraph

Review in Neurotoxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
–field-weighted citation impact
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

33 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Effect of PGEOncotarget · 2017
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. PGE2-EP3 signaling exacerbates intracerebral hemorrhage outcomes in 24-mo-old mice.American journal of physiology. Heart and circulatory physiology · 2016
    Article
  20. Article
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

3 authors.

Dejan MilatovicDepartment of Pediatrics, Division of Clinical Pharmacology and Toxicology, Vanderbilt University Medical Center, Nashville, TN 37232, USA. dejan.milatovic@vanderbilt.edu
Thomas J Montine
Michael Aschner

Funding

Mechanisms of Manganese NeurotoxicityR01ES010563 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 2001 to 2026
$11.9M
Mechanisms of Methylmercury Induced Neuron ToxicityR01ES007331 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI Michael Aschner, Aaron B Bowman · 1996 to 2026
$10.6M
Toxicants and innate immunity in models of Parkinson's diseaseR01ES016754 · NIEHS · UNIVERSITY OF WASHINGTON · PI MONTINE, THOMAS J · 2009 to 2013
$1.7M
Multidisciplinary Training in Molecular ToxicologyT32ES007331 · NIEHS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI TOWNSEND, ALAN J · 2001 to 2005
$1.3M
Anticholinesterase Neurotoxicity is Mediated by Oxidative InjuryR21NS057223 · NINDS · VANDERBILT UNIVERSITY · PI MILATOVIC, DEJAN · 2007 to 2008
$422k
NIEHS NIH HHS ES07331NIEHS NIH HHS ES10563NIEHS NIH HHS ES16754NIEHS NIH HHS R01 ES007331NIEHS NIH HHS R01 ES010563NIEHS NIH HHS R01 ES016754NIEHS NIH HHS T32 ES007331NINDS NIH HHS NS057223NINDS NIH HHS R21 NS057223
6 · The paper itself

Abstract

The prostanoids, a naturally occurring subclass of eicosanoids, are lipid mediators generated through oxidative pathways from arachidonic acid. These cyclooxygenase metabolites, consisting of the prostaglandins (PG), prostacyclin and tromboxane, are released in response to a variety of physiological and pathological stimuli in almost all organs, including the brain. They are produced by various cell types and act upon targeted cells via specific G protein-coupled receptors. The existence of multiple receptors, cross-reactivity and coupling to different signal transduction pathways for each prostanoid, collectively establish their diverse effects. Notably, these effects can occur in functionally opposing directions within the same cell or organ. Prostaglandin E(2) (PGE(2)) is the most versatile prostanoid because of its receptors, E Prostanoid (EP) receptor subtypes 1 through 4, its biological heterogeneity and its differential expression on neuronal and glial cells throughout the central nervous system. Since PGE(2) plays an important role in processes associated with various neurological diseases, this review focuses on its dual neuroprotective and neurotoxic role in EP receptor subtype signaling pathways in different models of brain injury.

Indexed as

Signal TransductionAnimalsBrainDinoprostoneHumansModels, AnimalNeurotoxicity SyndromesReceptors, Prostaglandin EDinoprostoneReceptors, Prostaglandin E

Identifiers

PMID21376752
PMCPMC3090136

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.