Evidence map›Paper›PMID 20206688›Full record

ArticleCellular signalling2010

Radiation-induced bystander signaling pathways in human fibroblasts: a role for interleukin-33 in the signal transmission.

Vladimir N Ivanov, Hongning Zhou, Shanaz A Ghandhi, Thomas B Karasic, Benjamin Yaghoubian, Sally A Amundson, Tom K Hei

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
8.7field-weighted citation impact, top 2% 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

48 citing papers in PubMed, 122 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Proregenerative Activity of IL-33 in Gastric Tissue Cells UndergoingInternational journal of molecular sciences · 2020
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. IL-33 facilitates proliferation of colorectal cancer dependent on COX2/PGEJournal of experimental & clinical cancer research : CR · 2018
    Article
  16. Review
  17. Article
  18. Review
  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

7 authors at 1 institution in 1 country.

Vladimir N IvanovCenter for Radiological Research, Department of Radiation Oncology, Columbia University, New York, NY 10032, USA. vni3@columbia.edu
Hongning Zhou
Shanaz A Ghandhi
Thomas B Karasic
Benjamin Yaghoubian
Sally A Amundson
Tom K Hei
Columbia University · US

Funding

THE FUNCTIONAL GENOMICS OF BYSTANDER RESPONSESP01CA049062 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HEI, TOM K. · 1990 to 2014
$21.9M
TR&D 3P41EB002033 · NIBIB · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BRENNER, DAVID JONATHAN · 2003 to 2018
$17.0M
Cytoplasmic Damage and GenotoxicityR01ES012888 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HEI, TOM K. · 2004 to 2016
$3.9M
NCI NIH HHS CA 49062NCI NIH HHS P01 CA049062NIBIB NIH HHS EB-002033NIBIB NIH HHS P41 EB002033NIEHS NIH HHS ES 012888-05S1NIEHS NIH HHS R01 ES012888
6 · The paper itself

Abstract

The main goal of this study is to elucidate the mechanisms of the signal transmission for radiation-induced bystander response. The NF-kappaB-dependent gene expression of IL8, IL6, PTGS2/COX2, TNF and IL33 in directly irradiated human skin fibroblasts produced the cytokines and prostaglandin E2 (PGE2) with autocrine/paracrine functions, which further activated signaling pathways and induced NF-kappaB-dependent gene expression in bystander cells. As a result, bystander cells also started expression and production of interleukin-8, interleukin-6, COX-2-generated PGE2 and interleukin-33 (IL-33) followed by autocrine/paracrine stimulation of the NF-kappaB and MAPK pathways. A blockage of IL-33 transmitting functions with anti-IL-33 monoclonal antibody added into the culture media decreased NF-kappaB activation in directly irradiated and bystander cells. On the other hand, the IGF-1-Receptor kinase regulated the PI3K-AKT pathway in both directly irradiated and bystander fibroblasts. A pronounced and prolonged increase in AKT activity after irradiation was a characteristic feature of bystander cells. AKT positively regulated IL-33 protein expression levels. Suppression of the IGF-R1-AKT-IL-33 pathway substantially increased radiation-induced or TRAIL-induced apoptosis in fibroblasts. Taken together, our results demonstrated the early activation of NF-kappaB-dependent gene expression first in directly irradiated and then bystander fibroblasts, the further modulation of critical proteins, including IL-33, by AKT in bystander cells and late drastic changes in cell survival and in enhanced sensitivity to TRAIL-induced apoptosis after suppression of the IGF-1R-AKT-IL-33 signaling cascade in both directly irradiated and bystander cells.

Indexed as

Signal TransductionApoptosisAtaxia Telangiectasia Mutated Proteinsbeta CateninBystander EffectCell Cycle ProteinsCell SurvivalCytokinesDNA-Binding ProteinsFibroblastsGene ExpressionHumansInsulin-Like Growth Factor Binding Protein 3Intercellular Signaling Peptides and ProteinsInterleukin-33InterleukinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanbeta CateninCell Cycle ProteinsCytokinesDNA-Binding ProteinsIL33 protein, humanInsulin-Like Growth Factor Binding Protein 3Intercellular Signaling Peptides and ProteinsInterleukin-33InterleukinsIntracellular Signaling Peptides and ProteinsMTOR protein, humanProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktReceptors, Growth FactorReceptors, SomatomedinTNF-Related Apoptosis-Inducing LigandTOR Serine-Threonine KinasesTumor Suppressor Proteins

Identifiers

PMID20206688
PMCPMC2860693
OpenAlexW2150022465

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.