Evidence map›Paper›PMID 21865854›Full record

ArticleCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology2011

NFĸB is an unexpected major mediator of interleukin-15 signaling in cerebral endothelia.

Kirsten P Stone, Abba J Kastin, Weihong Pan

Open access · bronzeAbstract read
In one paragraph

Article in Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.2field-weighted citation impact, top 10% 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

42 citing papers in PubMed, 63 citations in OpenAlex.

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  7. Theracurmin Modulates Cardiac Inflammation in Experimental Model ofTropical medicine and infectious disease · 2023
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  10. Review
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  14. Article
  15. Soluble CD163 Changes Indicate Monocyte Association With Cognitive Deficits in Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2021
    Article
  16. Strategies for Biomaterial-Based Spinal Cord Injury RepairFrontiers in bioengineering and biotechnology · 2021
    Review
  17. Article
  18. Review
  19. Article
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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

3 authors at 1 institution in 1 country.

Kirsten P StoneBlood-Brain Barrier Group, Pennington Biomedical Research Center, Baton Rouge, USA. kirsten.stone@pbrc.edu
Abba J Kastin
Weihong Pan
Pennington Biomedical Research Center · US

Funding

Leptin Transport Across the BBB: The Role of ObR (+) AstrocytesR01DK054880 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI KASTIN, ABBA J · 1999 to 2014
$4.4M
Neuroimmune modulation across the BBB: Regulation of ILS trafficking by TNFR01NS062291 · NINDS · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI PAN, WEIHONG · 2008 to 2012
$1.6M
Leptin Transport across the BBB: The Role of ObR (+) astrocytesR56DK054880 · NIDDK · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI KASTIN, ABBA J · 2010 to 2010
$222k
NIDDK NIH HHS DK54880NIDDK NIH HHS R01 DK054880NIDDK NIH HHS R56 DK054880NINDS NIH HHS NS62291NINDS NIH HHS R01 NS062291
6 · The paper itself

Abstract

Interleukin (IL)-15 and its receptors are induced by tumor necrosis factor α (TNF) in the cerebral endothelial cells composing the blood-brain barrier, but it is not yet clear how IL-15 modulates endothelial function. Contrary to the known induction of JAK/STAT3 signaling, here we found that nuclear factor (NF)- κB is mainly responsible for IL-15 actions on primary brain microvessel endothelial cells and cerebral endothelial cell lines. IL-15-induced transactivation of an NFκB luciferase reporter resulted in phosphorylation and degradation of the inhibitory subunit IκB that was followed by phosphorylation and nuclear translocation of the p65 subunit of NFκB. An IκB kinase inhibitor Bay 11-7082 only partially inhibited IL-15-induced NFκB luciferase activity. The effect of IL-15 was mediated by its specific receptor IL-15Rα, since endothelia from IL-15Rα knockout mice showed delayed nuclear translocation of p65, whereas those from knockout mice lacking a co-receptor IL-2Rγ did not show such changes. At the mRNA level, IL-15 and TNF showed similar effects in decreasing the tight junction protein claudin-2 and increasing the p65 subunit of NFκB but exerted different regulation on caveolin-1 and vimentin. Taken together, NFκB is a major signal transducer by which IL-15 affects cellular permeability, endocytosis, and intracellular trafficking at the level of the blood-brain barrier.

Indexed as

AnimalsBlood-Brain BarrierCaveolin 1Cells, CulturedCerebellumClaudinsEndothelial CellsEnzyme ActivationI-kappa B KinaseInterleukin-15Interleukin-15 Receptor alpha SubunitMiceMice, KnockoutNF-kappa BPhosphorylationSignal TransductionCaveolin 1ClaudinsCldn2 protein, mouseI-kappa B KinaseInterleukin-15Interleukin-15 Receptor alpha SubunitNF-kappa BSTAT3 Transcription FactorTranscription Factor RelATumor Necrosis Factor-alphaVimentin

Identifiers

PMID21865854
PMCPMC3709181
OpenAlexW2038245749

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.