Evidence map›Paper›PMID 19405838›Full record

ArticleJournal of periodontology2009

Expression profile of human gingival fibroblasts induced by interleukin-1beta reveals central role of nuclear factor-kappa B in stabilizing human gingival fibroblasts during inflammation.

Saynur Vardar-Sengul, Shilpi Arora, Haluk Baylas, Dan Mercola

Open access · greenAbstract read
In one paragraph

Article in Journal of periodontology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Microbiota in Periodontitis: Advances in the Omic Era.Advances in experimental medicine and biology · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Machine Learning with Optical Phase Signatures for Phenotypic Profiling of Cell Lines.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Atypical IκB proteins - nuclear modulators of NF-κB signaling.Cell communication and signaling : CCS · 2013
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 2 countries.

Saynur Vardar-SengulDepartment of Pathology and Laboratory Medicine, University of California, Irvine, Irvine, CA, USA.
Shilpi Arora
Haluk Baylas
Dan Mercola
University of California, Irvine · USEge University · TR

Funding

Evaluation of Predictive Signatures of Prostate CancerU01CA114810 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI MERCOLA, DAN · 2005 to 2009
$8.2M
NCI NIH HHS U01 CA114810NCI NIH HHS U01CA114810-03
6 · The paper itself

Abstract

backgroundInterleukin (IL)-1beta is a key cytokine in the pathogenesis of periodontitis, and it induces inflammatory mediators in periodontal diseases. We developed immortalized human gingival fibroblasts (HGFs), investigated the effects of IL-1beta on the gene expression using expression arrays containing approximately 40,000 genes, and tested the role of nuclear factor-kappa B (NF-kappaB) in maintaining an activated HGF population.

methodsTotal RNA was isolated from IL-1beta-induced and mock-induced control cells. Gene expression analyses were performed using expression arrays and confirmed by quantitative real-time polymerase chain reaction. Western blot analysis to show inhibitor of kappa B-alpha (IkappaBalpha) phosphorylation and immunostaining of cells for NF-kappaB nuclear translocation were performed. Apoptosis was confirmed by assay of poly ADP-ribose polymerase (PARP) cleavage.

resultsA total of 382 probe sets corresponding to 254 genes were differentially expressed in IL-1beta-induced cells (P <0.001). A total of 215 genes were upregulated, and 39 genes were downregulated. Most notable NF-kappaB pathway members (NFkappaB1, NFkappaB2, IkappaBalpha, IkappaBepsilon, IkappaBzeta, REL, RELB, and TA-NFKBH) were upregulated. IkappaBalpha was phosphorylated, and NF-kappaB accumulated in the nucleus. An IL-1beta-induced set of 27 genes was downregulated by an NF-kappaB inhibitor, leading to a decreased number of viable cells and suggesting an antiapoptotic role for NF-kappaB.

conclusionsIL-1beta leads to a large number of significant expression changes consistent with a pathologic role in periodontitis, including enhancement of inflammatory cytokines, chemokines, transcription factors, matrix metalloproteinases, adhesion molecules, and especially NF-kappaB-dependent antiapoptotic genes. NF-kappaB activation blocks apoptosis, thereby stabilizing the HGF population in inflammation.

Indexed as

Gene Expression ProfilingActive Transport, Cell NucleusApoptosisCell Line, TransformedDown-RegulationFibroblastsGene Expression RegulationGingivaGingivitisHumansI-kappa B ProteinsInterleukin-1betaMAP Kinase Signaling SystemNF-kappa BNF-KappaB Inhibitor alphaOligonucleotide Array Sequence AnalysisI-kappa B ProteinsInterleukin-1betaNF-kappa BNF-KappaB Inhibitor alphaNFKBIA protein, human

Identifiers

PMID19405838
PMCPMC4150685
OpenAlexW2010628368

What OpenQuestion holds

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Registered trials

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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.