Evidence map›Paper›PMID 18208539›Full record

ArticleJournal of neurochemistry2008

Transcription factor early growth response-1 induction mediates inflammatory gene expression and brain damage following transient focal ischemia.

Kudret Tureyen, Nathaniel Brooks, Kellie Bowen, John Svaren, Raghu Vemuganti

Open access · greenAbstract readComparative Study
In one paragraph

Article in Journal of neurochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. A role for astrocytic insulin-like growth factor I receptors in the response to ischemic insult.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. CCL26 regulates the proportion of CD4Experimental and therapeutic medicine · 2020
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Observational
  19. Long Noncoding RNA FosDT Promotes Ischemic Brain Injury by Interacting with REST-Associated Chromatin-Modifying Proteins.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    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

5 authors at 2 institutions in 2 countries.

Kudret TureyenDepartment of Neurological Surgery, University of Wisconsin, Madison, Wisconsin 53792, USA.
Nathaniel Brooks
Kellie Bowen
John Svaren
Raghu Vemuganti
Neurological Surgery · USUniversity of Wisconsin–Madison · US

Funding

Genetic Control of Myelination by EGR2 and NAB proteinsR01HD041590 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI SVAREN, JOHN P · 2002 to 2011
$2.8M
Role of Egr-1 in post-stroke inflammation & brain damageR01NS049448 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI VEMUGANTI, RAGHU · 2006 to 2009
$1.0M
Transcription Factors &Inflammatory Mediators in StrokeR01NS044173 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI VEMUGANTI, RAGHU · 2004 to 2007
$792k
NICHD NIH HHS R01 HD041590NINDS NIH HHS R01 NS044173NINDS NIH HHS R01 NS049448
6 · The paper itself

Abstract

Early growth response-1 (Egr1) is a sequence-specific transcription factor (TF) which is induced under hypoxic conditions. We presently report that transient middle cerebral artery occlusion (MCAO) leads to increased expression of Egr1 in the brains of adult mice and rats between 2 h and 5 days of reperfusion with a peak increase of 8-12-fold at 1 day. When subjected to transient MCAO and 3 days of reperfusion, Egr1-/- mice showed significantly smaller infarcts (by 44.9 +/- 8.4%, p < 0.05) and improved neurological function than Egr1+/+ littermates. Following transient MCAO, brains of Egr1-/- mice showed less water accumulation and decreased neutrophil infiltration (by 42 +/- 8%, p < 0.05) compared to Egr1+/+ mice. The number of activated microglia/macrophages were also significantly lower (OX42+ cells by 53 +/- 9%, p < 0.05 and ED1+ cells by 59 +/- 11%) in the post-ischemic cortex of Egr1-/- mice compared to Egr1+/+ mice. In addition, post-ischemic inflammatory gene expression was less pronounced in the brains of Egr1-/- mice compared to Egr1+/+ mice. Preventing cerebral Egr1 protein induction with small interference RNAs that target Egr1 decreased inflammatory gene expression and led to smaller infarcts (by 40.2 +/- 6.9%, p < 0.05) and reduced neurological deficits in rats subjected to transient MCAO. Conversely, transient MCAO following adenoviral-mediated Egr1 over-expression exacerbated the infarct volume (by 29 +/- 5.3%, p < 0.05) and worsened the neurological deficits in rats. These studies indicate Egr1 as a significant contributor of inflammation and neuronal damage after stroke.

Indexed as

AnimalsCell LineEarly Growth Response Protein 1Gene Expression RegulationHumansHypoxia, BrainInflammation MediatorsIschemic Attack, TransientMiceMice, Inbred C57BLMice, KnockoutRatsRats, Inbred SHRTranscription FactorsEarly Growth Response Protein 1Egr1 protein, mouseInflammation MediatorsTranscription Factors

Identifiers

PMID18208539
PMCPMC2603292
OpenAlexW1987595468

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.