Evidence map›Paper›PMID 18545259›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2008

Role of the p38 mitogen-activated protein kinase/cytosolic phospholipase A2 signaling pathway in blood-brain barrier disruption after focal cerebral ischemia and reperfusion.

Chikako Nito, Hiroshi Kamada, Hidenori Endo, Kuniyasu Niizuma, D Jeannie Myer, Pak H Chan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
7.7field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 125 citations in OpenAlex.

  1. Article
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  9. Article
  10. Functions and mechanisms of cytosolic phospholipase ANeural regeneration research · 2023
    Review
  11. Article
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  18. Article
  19. Functions of p38 MAP Kinases in the Central Nervous System.Frontiers in molecular neuroscience · 2020
    Review
  20. Article

11 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 1 institution in 1 country.

Chikako NitoDepartment of Neurosurgery, Stanford University School of Medicine, Stanford, California 94305-5487, USA. chnagata@sk9.so-net.ne.jp
Hiroshi Kamada
Hidenori Endo
Kuniyasu Niizuma
D Jeannie Myer
Pak H Chan
Stanford University · US

Funding

Transgenic Animal CoreP50NS014543 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI GIFFARD, RONA G · 1990 to 2007
$8.2M
Reperfusion and Neurovascular Injury in StrokeR01NS025372 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1988 to 2015
$5.0M
Cell Death/Survival After Global Cerebral IschemiaR01NS038653 · NINDS · STANFORD UNIVERSITY · PI CHAN, PAK H · 1998 to 2013
$4.5M
OXYGEN RADICALS AND NEURONAL APOPTOSIS IN FOCAL STROKER01NS036147 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1997 to 2010
$3.8M
NINDS NIH HHS P50 NS014543NINDS NIH HHS R01 NS025372NINDS NIH HHS R01 NS036147NINDS NIH HHS R01 NS038653
6 · The paper itself

Abstract

Cytosolic phospholipase A(2) (cPLA(2)) is a key enzyme that mediates arachidonic acid metabolism, which causes cerebral ischemia-induced oxidative injury, blood-brain barrier (BBB) dysfunction, and edema. Recent reports have shown that p38 mitogen-activated protein kinase (MAPK) is related to phosphorylation and activation of cPLA(2) and release of arachidonic acid. However, involvement of the p38 MAPK pathway in cPLA(2) activation and of reactive oxygen species in expression of p38 MAPK/cPLA(2) after ischemia-reperfusion injury in the brain remains unclear. To address these issues, we used a model of transient focal cerebral ischemia (tFCI) in rats. Western blot analysis showed a significant increase in expression of phospho-p38 MAPK and phospho-cPLA(2) in rat brain cortex after tFCI. Activity assays showed that both p38 MAPK and cPLA(2) activation markedly increased 1 day after reperfusion. Intraventricular administration of SB203580 significantly suppressed activation and phosphorylation of cPLA(2) and attenuated BBB extravasation and subsequent edema. Moreover, overexpression of copper/zinc-superoxide dismutase remarkably diminished activation and phosphorylation of both p38 MAPK and cPLA(2) after reperfusion. These findings suggest that the p38 MAPK/cPLA(2) pathway may promote BBB disruption with secondary vasogenic edema and that superoxide anions can stimulate this pathway after ischemia-reperfusion injury.

Indexed as

AnimalsAnimals, Genetically ModifiedBlood-Brain BarrierBrain EdemaBrain IschemiaCerebral InfarctionCyclooxygenase 2Enzyme InhibitorsHumansImidazolesMaleOxidative Stressp38 Mitogen-Activated Protein KinasesPhospholipases A2, CytosolicPhosphorylationPyridinesCyclooxygenase 2Enzyme InhibitorsImidazolesp38 Mitogen-Activated Protein KinasesPhospholipases A2, CytosolicPtgs2 protein, ratPyridinesSB 203580SOD1 protein, humanSod1 protein, ratSuperoxide DismutaseSuperoxide Dismutase-1Superoxides

Identifiers

PMID18545259
PMCPMC2562626
OpenAlexW2022642913

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.