Evidence map›Paper›PMID 23032483›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2013

Prevention of JNK phosphorylation as a mechanism for rosiglitazone in neuroprotection after transient cerebral ischemia: activation of dual specificity phosphatase.

Nobuya Okami, Purnima Narasimhan, Hideyuki Yoshioka, Hiroyuki Sakata, Gab Seok Kim, Joo Eun Jung, Carolina M Maier, 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, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  6. Review
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  11. The neuroprotective effects ofChinese medicine · 2017
    Article
  12. Article
  13. Curcumin attenuates ischemia-like injury induced IL-1β elevation in brain microvascular endothelial cells via inhibiting MAPK pathways and nuclear factor-κB activation.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2014
    Article
  14. Article
  15. 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

8 authors at 1 institution in 1 country.

Nobuya OkamiDepartment of Neurosurgery, Department of Neurology and Neurological Sciences, and Program in Neurosciences, Stanford University School of Medicine, Stanford, CA, USA.
Purnima Narasimhan
Hideyuki Yoshioka
Hiroyuki Sakata
Gab Seok Kim
Joo Eun Jung
Carolina M Maier
Pak H Chan
Stanford University · US

Funding

Reperfusion and Neurovascular Injury in StrokeR01NS025372 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI CHAN, PAK H · 1988 to 2015
$5.0M
Transgenic Animal CoreP01NS014543 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI GIFFARD, RONA G · 1985 to 2011
$4.7M
Cell Death/Survival After Global Cerebral IschemiaR01NS038653 · NINDS · STANFORD UNIVERSITY · PI CHAN, PAK H · 1998 to 2013
$4.5M
NINDS NIH HHS P01 NS014543NINDS NIH HHS R01 NS025372NINDS NIH HHS R01 NS038653
6 · The paper itself

Abstract

Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-γ (PPARγ) agonist, prevents cell death after cerebral ischemia in animal models, but the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone protects neurons against ischemia. Mice treated with rosiglitazone were subjected to 60 minutes of focal ischemia followed by reperfusion. Rosiglitazone reduced infarct volume after ischemia and reperfusion. We show that this neuroprotective effect was reversed with a PPARγ antagonist. Western blot analysis showed a significant increase in expression of phosphorylated stress-activated protein kinases (c-Jun N-terminal kinase (JNK) and p38) in ischemic brain tissue. Rosiglitazone blocked this increase. Furthermore, we observed that rosiglitazone increased expression of the dual-specificity phosphatase 8 (DUSP8) protein and messenger RNA in ischemic brain tissue. Dual-specificity phosphatase 8 is a mitogen-activated protein kinase phosphatase that can dephosphorylate JNK and p38. Another key finding of the present study was that knockdown of DUSP8 in primary cultured cortical neurons that were subjected to oxygen-glucose deprivation diminished rosiglitazone's effect on downregulation of JNK phosphorylation. Thus, rosiglitazone's neuroprotective effect after ischemia is mediated by blocking JNK phosphorylation induced by ischemia via DUSP8 upregulation.

Indexed as

AnimalsBlotting, WesternCell DeathDisease Models, AnimalDual-Specificity PhosphatasesEnzyme ActivationGlucoseIschemic Attack, TransientJNK Mitogen-Activated Protein KinasesMaleMiceMice, Inbred C57BLNeuronsNeuroprotective AgentsOxygenPhosphorylationDual-Specificity PhosphatasesDUSP8 protein, mouseGlucoseJNK Mitogen-Activated Protein KinasesNeuroprotective AgentsOxygenPPAR gammaRosiglitazoneThiazolidinediones

Identifiers

PMID23032483
PMCPMC3597369
OpenAlexW2068689480

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.