Evidence map›Paper›PMID 18381429›Full record

ArticleCancer research2008

Mitochondrial function and nuclear factor-kappaB-mediated signaling in radiation-induced bystander effects.

Hongning Zhou, Vladimir N Ivanov, Yu-Chin Lien, Mercy Davidson, Tom K Hei

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 164 citations in OpenAlex.

  1. Radiomitigators: Breakthroughs in Post-Radiation Recovery.Antioxidants (Basel, Switzerland) · 2026
    Review
  2. Review
  3. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Mitochondrial Signaling Pathways Associated with DNA Damage Responses.International journal of molecular sciences · 2023
    Review
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  7. Review
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21 more citing papers are in PubMed but not listed here.

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 2 countries.

Hongning ZhouCenter for Radiological Research, College of Physicians and Surgeons, Mailman School of Public Health, Columbia University, New York, NY, USA.
Vladimir N Ivanov
Yu-Chin Lien
Mercy Davidson
Tom K Hei
Columbia University · USRoyal College of Physicians · GB

Funding

THE FUNCTIONAL GENOMICS OF BYSTANDER RESPONSESP01CA049062 · NCI · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HEI, TOM K. · 1990 to 2014
$21.9M
Cytoplasmic Damage and GenotoxicityR01ES012888 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI HEI, TOM K. · 2004 to 2016
$3.9M
VISUAL OF DNA DAMAGE PROCESS AFTER SINGLE PART TRAVERSALP41RR011623 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI BRENNER, DAVID JONATHAN · 1996 to 2002
$2.8M
NCI NIH HHS CA 11623NCI NIH HHS CA 49062NCI NIH HHS P01 CA049062NCRR NIH HHS P41 RR011623NIEHS NIH HHS ES 12888NIEHS NIH HHS R01 ES012888
6 · The paper itself

Abstract

Although radiation-induced bystander effects have been well described over the past decade, the mechanisms of the signaling processes involved in the bystander phenomenon remain unclear. In the present study, using the Columbia University charged particle microbeam, we found that mitochondrial DNA-depleted human skin fibroblasts (rho(o)) showed a higher bystander mutagenic response in confluent monolayers when a fraction of the same population were irradiated with lethal doses compared with their parental mitochondrial-functional cells (rho(+)). However, using mixed cultures of rho(o) and rho(+) cells and targeting only one population of cells with a lethal dose of alpha-particles, a decreased bystander mutagenesis was uniformly found in nonirradiated bystander cells of both cell types, indicating that signals from one cell type can modulate expression of bystander response in another cell type. In addition, we found that Bay 11-7082, a pharmacologic inhibitor of nuclear factor-kappaB (NF-kappaB) activation, and 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, a scavenger of nitric oxide (NO), significantly decreased the mutation frequency in both bystander rho(o) and rho(+) cells. Furthermore, we found that NF-kappaB activity and its dependent proteins, cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS), were lower in bystander rho(o) cells when compared with their rho(+) counterparts. Our results indicated that mitochondria play an important role in the regulation of radiation-induced bystander effects and that mitochondria-dependent NF-kappaB/iNOS/NO and NF-kappaB/COX-2/prostaglandin E2 signaling pathways are important to the process.

Indexed as

Alpha ParticlesAntibodies, MonoclonalBenzoatesCell CommunicationCells, CulturedCyclooxygenase 2DNA, MitochondrialFibroblastsHumansHypoxanthine PhosphoribosyltransferaseImidazolesLungMitochondriaMutagenesisNF-kappa BNitric Oxide Synthase Type II1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole3-(4-methylphenylsulfonyl)-2-propenenitrileAntibodies, MonoclonalBenzoatesCyclooxygenase 2DNA, MitochondrialHypoxanthine PhosphoribosyltransferaseImidazolesNF-kappa BNitric Oxide Synthase Type IINitrilesNOS2 protein, humanSulfonesTumor Necrosis Factor-alpha

Identifiers

PMID18381429
PMCPMC3715144
OpenAlexW2153080177

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.