Evidence map›Paper›PMID 24301291›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2014

A new role for downstream Toll-like receptor signaling in mediating immediate early gene expression during focal cerebral ischemia.

Bolanle M Famakin, Yongshan Mou, Kory Johnson, Maria Spatz, John Hallenbeck

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Yin and Yang of innate immunity in stroke.BioMed research international · 2014
    Review
  8. 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

5 authors at 2 institutions in 1 country.

Bolanle M FamakinNational Institute of Neurological Disorders and Stroke, Stroke Branch, National Institutes of Health, Bethesda, Maryland, USA.
Yongshan MouNational Institute of Neurological Disorders and Stroke, Stroke Branch, National Institutes of Health, Bethesda, Maryland, USA.
Kory JohnsonNational Institute of Neurological Disorders & Stroke, Section on Bioinformatics, Information Technology & Bioinformatics Program, National Institutes of Health, Bethesda, Maryland, USA.
Maria SpatzNational Institute of Neurological Disorders and Stroke, Stroke Branch, National Institutes of Health, Bethesda, Maryland, USA.
John HallenbeckNational Institute of Neurological Disorders and Stroke, Stroke Branch, National Institutes of Health, Bethesda, Maryland, USA.
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · US

Funding

Protective Mechanisms In Cerebral IschemiaZIANS002924 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HALLENBECK, JOHN · 2009 to 2018
$16.5M
Intramural NIH HHS
6 · The paper itself

Abstract

To better understand the role of downstream Toll-like receptor (TLR) signaling during acute cerebral ischemia, we performed cDNA microarrays, on brain RNA, and cytokine arrays, on serum, from wild type (WT), MyD88-/- and TRIF-mutant mice, at baseline and following permanent middle cerebral artery occlusion (pMCAO). The acute stress response pathway was among the top pathways identified by Ingenuity Pathway Analysis of microarray data. We used real-time polymerase chain reaction to confirm the expression of four immediate early genes; EGR1, EGR2, ARC, Nurr77, in this pathway, and insulin degrading enzyme (IDE). Compared to WT, baseline immediate early gene expression was increased up to10-fold in MyD88-/- and TRIF-mutant mice. However, following pMCAO, immediate early gene expression remained unchanged, from this elevated baseline in these mice, but increased up to 12-fold in WT. Furthermore, expression of IDE, which also degrades β-amyloid, decreased significantly only in TRIF-mutant mice. Finally, sE-Selectin, sICAM, sVCAM-1, and MMP-9 levels were significantly decreased only in MyD88-/- compared with WT mice. We thus report a new role for downstream TLR signaling in immediate early gene expression during acute cerebral ischemia. We also show that the TRIF pathway regulates IDE expression; a major enzyme that clears β-amyloid from the brain.

Indexed as

Signal TransductionAcute DiseaseAdaptor Proteins, Vesicular TransportAmyloid beta-PeptidesAnimalsBrain IschemiaCell Adhesion MoleculesCytoskeletal ProteinsEarly Growth Response Protein 1Early Growth Response Protein 2Gene Expression Regulation, EnzymologicInsulysinMatrix Metalloproteinase 9MiceMice, KnockoutMyeloid Differentiation Factor 88activity regulated cytoskeletal-associated proteinAdaptor Proteins, Vesicular TransportAmyloid beta-PeptidesCell Adhesion MoleculesCytoskeletal ProteinsEarly Growth Response Protein 1Early Growth Response Protein 2Egr1 protein, mouseEgr2 protein, mouseInsulysinMatrix Metalloproteinase 9Mmp9 protein, mouseMyd88 protein, mouseMyeloid Differentiation Factor 88Nerve Tissue ProteinsTicam1 protein, mouseToll-Like Receptors

Identifiers

PMID24301291
PMCPMC3915199
OpenAlexW2012657344

What OpenQuestion holds

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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.