Evidence map›Paper›PMID 22323467›Full record

ArticleInvestigative ophthalmology & visual science2012

NF-κB is the transcription factor for FGF-2 that causes endothelial mesenchymal transformation in cornea.

Jeong Goo Lee, EunDuck P Kay

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
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  10. Injured Endothelial Cell: A Risk Factor for Pulmonary Fibrosis.International journal of molecular sciences · 2023
    Review
  11. Review
  12. Review
  13. Inhalation of Tungsten Metal Particulates Alters the Lung and Bone Microenvironments Following Acute Exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Diseases of the corneal endothelium.Experimental eye research · 2021
    Review
  19. Review
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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

2 authors at 1 institution in 1 country.

Jeong Goo LeeDoheny Eye Institute, Keck School of Medicine of the University of Southern California, Los Angeles, California, USA.
EunDuck P Kay
Doheny Eye Institute · US

Funding

VISION RESEARCHP30EY003040 · NEI · DOHENY EYE INSTITUTE · PI SUN, DEMING · 1985 to 2013
$7.0M
STUDIES ON MECHANISM OF RETROCORNEAL FIBROUS MEMBRANE INR01EY006431 · NEI · UNIVERSITY OF TEXAS SW MED CTR/DALLAS · PI KAY, EUNDUCK P · 1985 to 2010
$3.9M
NEI NIH HHS EY03040NEI NIH HHS EY06431NEI NIH HHS P30 EY003040NEI NIH HHS R01 EY006431
6 · The paper itself

Abstract

purposeTo determine the role of nuclear factor-κB (NF-κB) during FGF-2-mediated endothelial mesenchymal transformation (EMT) in response to interleukin (IL)-1β stimulation in corneal endothelial cells (CECs).

methodsExpression and/or activation of IL-1 receptor-associated protein kinase (IRAK), TNF receptor-associated factor 6 (TRAF6), phosphatidylinositol 3-kinase (PI 3-kinase), IκB kinase (IKK), IκB, NF-κB, and FGF-2 were analyzed by immunoblot analysis. Cell proliferation was measured by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. NF-κB activity was measured by NF-κB ELISA kit, while binding of NF-κB to the promoter region of FGF-2 gene was determined by chromatin immunoprecipitation.

resultsBrief stimulation of CECs with IL-1β upregulated expression of IRAK and TRAF6 and activated PI 3-kinase; expression of IRAK and TRAF6 reached maximum within 60 minutes, after which the expression disappeared, while PI 3-kinase activity was observed up to 4 hours after IL-1β stimulation. Use of specific inhibitor to PI 3-kinase or IRAK demonstrated that IRAK activates PI 3-kinase, the signaling of which phosphorylates IKKα/β and degrades IκB, subsequently leading to activation of NF-κB. The induction of FGF-2 by IL-1β was completely blocked by inhibitors to NF-κB activation (sulfasalazine) or PI 3-kinase (LY294002), and both inhibitors greatly blocked cell proliferation of CECs. Chromatin immunoprecipitation further demonstrated that NF-κB is the transcription factor of FGF-2 as NF-κB binds the putative NF-κB binding site of the FGF-2 promoter.

conclusionsThese data suggest that IL-1β signaling combines the canonical pathway and the PI 3-kinase signaling to upregulate FGF-2 production through NF-κB, which plays a key role as a transcription factor of FGF-2 gene.

Indexed as

AnimalsCell ProliferationCells, CulturedChromatinEndothelium, CornealEnzyme-Linked Immunosorbent AssayEpithelial-Mesenchymal TransitionFibroblast Growth Factor 2HumansI-kappa B KinaseImmunoblottingInterleukin-1betaInterleukin-1 Receptor-Associated KinasesNF-kappa BPhosphatidylinositol 3-KinasesRabbitsChromatinFibroblast Growth Factor 2I-kappa B KinaseInterleukin-1betaInterleukin-1 Receptor-Associated KinasesNF-kappa BPhosphatidylinositol 3-KinasesTNF Receptor-Associated Factor 6

Identifiers

PMID22323467
PMCPMC3339915
OpenAlexW2022194518

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.