Evidence map›Paper›PMID 19234157›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2009

Transgenic inhibition of astroglial NF-kappa B improves functional outcome in experimental autoimmune encephalomyelitis by suppressing chronic central nervous system inflammation.

Roberta Brambilla, Trikaldarshi Persaud, Xianchen Hu, Shaffiat Karmally, Valery I Shestopalov, Galina Dvoriantchikova, Dmitry Ivanov, Lubov Nathanson, Scott R Barnum, John R Bethea

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 261 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

106 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

10 authors at 4 institutions in 2 countries.

Roberta BrambillaThe Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, 1095 Northwest 14th Terrace, Miami, FL 33136, USA. r.brambilla@miami.edu
Trikaldarshi Persaud
Xianchen Hu
Shaffiat Karmally
Valery I Shestopalov
Galina Dvoriantchikova
Dmitry Ivanov
Lubov Nathanson
Scott R Barnum
John R Bethea
The California Eye Institute · USUniversity of Alabama at Birmingham · USUniversity of Miami · USVavilov Institute of General Genetics · RU

Funding

TNF in Injury and Repair Processes Following Traumatic SCIR01NS051709 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI John Roland Bethea · 2005 to 2026
$8.0M
Astrocytes Play a Critical Role in the Pathology of EAER01NS065479 · NINDS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI BETHEA, JOHN ROLAND · 2009 to 2013
$1.6M
The Role of C3 and C3 receptors in Experimental Autoimmune EncephalomyelitisR01NS046032 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BARNUM, SCOTT R · 2004 to 2007
$1.2M
The role of NFkB in glia-neuron crosstalk in glaucomaR21EY017991 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2007 to 2008
$401k
NEI NIH HHS EY017991NEI NIH HHS R21 EY017991NINDS NIH HHS NS051709NINDS NIH HHS NS46032NINDS NIH HHS R01 NS046032NINDS NIH HHS R01 NS051709NINDS NIH HHS R01 NS065479
6 · The paper itself

Abstract

In the CNS, the transcription factor NF-kappaB is a key regulator of inflammation and secondary injury processes. Following trauma or disease, the expression of NF-kappaB-dependent genes is activated, leading to both protective and detrimental effects. In this study, we show that transgenic inactivation of astroglial NF-kappaB (glial fibrillary acidic protein-IkappaB alpha-dominant-negative mice) resulted in reduced disease severity and improved functional recovery following experimental autoimmune encephalomyelitis. At the chronic stage of the disease, transgenic mice exhibited an overall higher presence of leukocytes in spinal cord and brain, and a markedly higher percentage of CD8(+)CD122(+) T regulatory cells compared with wild type, which correlated with the timing of clinical recovery. We also observed that expression of proinflammatory genes in both spinal cord and cerebellum was delayed and reduced, whereas the loss of neuronal-specific molecules essential for synaptic transmission was limited compared with wild-type mice. Furthermore, death of retinal ganglion cells in affected retinas was almost abolished, suggesting the activation of neuroprotective mechanisms. Our data indicate that inhibiting NF-kappaB in astrocytes results in neuroprotective effects following experimental autoimmune encephalomyelitis, directly implicating astrocytes in the pathophysiology of this disease.

Indexed as

AnimalsAstrocytesCentral Nervous SystemChronic DiseaseEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression ProfilingGlial Fibrillary Acidic ProteinI-kappa B ProteinsInflammation MediatorsMaleMiceMice, TransgenicNF-kappa BNF-KappaB Inhibitor alphaOligonucleotide Array Sequence AnalysisGlial Fibrillary Acidic ProteinI-kappa B ProteinsInflammation MediatorsNF-kappa BNF-KappaB Inhibitor alphaNfkbia protein, mouse

Identifiers

PMID19234157
PMCPMC4291126
OpenAlexW1639462457

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.