Evidence map›Paper›PMID 19439596›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Neuronal PPARgamma deficiency increases susceptibility to brain damage after cerebral ischemia.

Xiurong Zhao, Roger Strong, Jie Zhang, Guanghua Sun, Joe Z Tsien, Zhenzhong Cui, James C Grotta, Jaroslaw Aronowski

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
5.9field-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

91 citing papers in PubMed, 162 citations in OpenAlex.

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31 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

8 authors at 3 institutions in 1 country.

Xiurong ZhaoStroke Program, Department of Neurology, University of Texas, Houston, Medical School, Houston, Texas 77030, USA.
Roger Strong
Jie Zhang
Guanghua Sun
Joe Z Tsien
Zhenzhong Cui
James C Grotta
Jaroslaw Aronowski
The University of Texas Health Science Center at Houston · USAugusta University · USNational Institute of Mental Health · US

Funding

New Target For Stroke: Peroxisome Proliferator Activated Receptor-GammaR01NS052791 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ARONOWSKI, JAROSLAW · 2006 to 2008
$874k
Pparg In Macrophage Promote Hematoma Absorption After Intracerebral HemorrhageR21NS057284 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI ZHAO, XIURONG · 2007 to 2008
$357k
NINDS NIH HHS 1R21NS057284NINDS NIH HHS R01 NS052791NINDS NIH HHS R01NS052791NINDS NIH HHS R21 NS057284
6 · The paper itself

Abstract

Peroxisome proliferator-activated receptor gamma (PPARgamma) plays a role in regulating a myriad of biological processes in virtually all brain cell types, including neurons. We and others have reported recently that drugs which activate PPARgamma are effective in reducing damage to brain in distinct models of brain disease, including ischemia. However, the cell type responsible for PPARgamma-mediated protection has not been established. In response to ischemia, PPARgamma gene is robustly upregulated in neurons, suggesting that neuronal PPARgamma may be a primary target for PPARgamma-agonist-mediated neuroprotection. To understand the contribution of neuronal PPARgamma to ischemic injury, we generated conditional neuron-specific PPARgamma knock-out mice (N-PPARgamma-KO). These mice are viable and appeared to be normal with respect to their gross behavior and brain anatomy. However, neuronal PPARgamma deficiency caused these mice to experience significantly more brain damage and oxidative stress in response to middle cerebral artery occlusion. The primary cortical neurons harvested from N-PPARgamma-KO mice, but not astroglia, exposed to ischemia in vitro demonstrated more damage and a reduced expression of numerous key gene products that could explain increased vulnerability, including SOD1 (superoxide dismutase 1), catalase, glutathione S-transferase, uncoupling protein-1, or transcription factor liver X receptor-alpha. Also, PPARgamma agonist-based neuroprotective effect was lost in neurons from N-PPARgamma neurons. Therefore, we conclude that PPARgamma in neurons play an essential protective function and that PPARgamma agonists may have utility in neuronal self-defense, in addition to their well established anti-inflammatory effect.

Indexed as

AnimalsAstrocytesBrainCells, CulturedCoculture TechniquesFemaleGene ExpressionInfarction, Middle Cerebral ArteryMaleMiceMice, Inbred C57BLMice, KnockoutNeurogliaNeuronsNeuroprotective AgentsOxidative StressNeuroprotective AgentsPPAR gammaRNA, MessengerRosiglitazoneThiazolidinediones

Identifiers

PMID19439596
PMCPMC2739014
OpenAlexW2079209433

What OpenQuestion holds

Textmetadata
LicenceTDM
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.