Evidence map›Paper›PMID 19107136›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2009

Mucosal tolerance to E-selectin promotes the survival of newly generated neuroblasts via regulatory T-cell induction after stroke in spontaneously hypertensive rats.

Satoru Ishibashi, Dragan Maric, Yongshan Mou, Ryo Ohtani, Christl Ruetzler, John M Hallenbeck

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, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.9field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Regulatory T cells in ischemic stroke.Acta pharmacologica Sinica · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Regulatory T Cells in Post-stroke Immune Homeostasis.Translational stroke research · 2016
    Review
  17. Inflammatory Disequilibrium in Stroke.Circulation research · 2016
    Review
  18. Review
  19. Article
  20. Review
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 2 institutions in 2 countries.

Satoru IshibashiStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health (NIH), Bethesda, Maryland 20892-4476, USA.
Dragan Maric
Yongshan Mou
Ryo Ohtani
Christl Ruetzler
John M Hallenbeck
National Institutes of Health · USNational Institute of Neurological Disorders and Stroke · US

Funding

Protective Mechanisms In Cerebral IschemiaZIANS002924 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HALLENBECK, JOHN · 2009 to 2018
$16.5M
PROTECTIVE MECHANISMS IN CEREBRAL ISCHEMIAZ01NS002924 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI HALLENBECK, JOHN M · 1996 to 2008
$3.6M
Intramural NIH HHS Z01 NS002924
6 · The paper itself

Abstract

Neuroblasts in the subventricular zone (SVZ) proliferate markedly after brain ischemia, and migrate to the site of injury along with blood vessels. However, a large fraction of stroke-generated neuroblasts die shortly after being born, in part, because of local inflammation. In spontaneously hypertensive rats (SHRs) subjected to permanent middle cerebral artery occlusion, we primed E-selectin-specific regulatory T cells (Tregs) by repetitive intranasal administration of recombinant E-selectin to target local secretion of immunomodulating, antiinflammatory cytokines to activating blood vessel segments. E-selectin-tolerized SHRs had decreased infarction volumes, and increased numbers of Tregs in the cervical lymph nodes and ischemic brain. The brain Tregs were distributed primarily in periinfarct regions. E-selectin tolerization did not alter cellular proliferation in the ipsilateral SVZ after stroke, but the expression of tumor necrosis factor on vascular niche blood vessels was suppressed and both doublecortin protein levels and the number of newly generated neuroblasts or neurons were increased in the brain. This enhanced survival of neural progenitor cells and neurons was paralleled by improved functional performance. These studies suggest that E-selectin-specific Tregs can modulate the efficacy of neurogenesis after ischemia and promote repair after brain injury.

Indexed as

Administration, IntranasalAnimalsCell DeathCytokinesDisease Models, AnimalDoublecortin ProteinE-SelectinImmune ToleranceImmunity, MucosalInfarction, Middle Cerebral ArteryNasal MucosaNeuronsRatsRats, Inbred SHRRecombinant ProteinsStem CellsCytokinesDcx protein, ratDoublecortin ProteinE-SelectinRecombinant Proteins

Identifiers

PMID19107136
PMCPMC2692388
OpenAlexW1990626639

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.