Document Detail


Mitochondrial function and nuclear factor-kappaB-mediated signaling in radiation-induced bystander effects.
MedLine Citation:
PMID:  18381429     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Hongning Zhou; Vladimir N Ivanov; Yu-Chin Lien; Mercy Davidson; Tom K Hei
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Cancer research     Volume:  68     ISSN:  1538-7445     ISO Abbreviation:  Cancer Res.     Publication Date:  2008 Apr 
Date Detail:
Created Date:  2008-04-02     Completed Date:  2008-04-25     Revised Date:  2013-09-01    
Medline Journal Info:
Nlm Unique ID:  2984705R     Medline TA:  Cancer Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2233-40     Citation Subset:  IM    
Affiliation:
Center for Radiological Research, College of Physicians and Surgeons, Mailman School of Public Health, Columbia University, New York, NY, USA.
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MeSH Terms
Descriptor/Qualifier:
Alpha Particles*
Antibodies, Monoclonal / immunology,  pharmacology
Benzoates / pharmacology
Cell Communication / physiology,  radiation effects
Cells, Cultured
Cyclooxygenase 2 / biosynthesis,  metabolism
DNA, Mitochondrial / metabolism
Fibroblasts / cytology,  drug effects,  metabolism,  radiation effects
Humans
Hypoxanthine Phosphoribosyltransferase / genetics,  metabolism
Imidazoles / pharmacology
Lung / cytology
Mitochondria / drug effects,  physiology*,  radiation effects*
Mutagenesis / drug effects,  radiation effects
NF-kappa B / antagonists & inhibitors,  metabolism*
Nitric Oxide Synthase Type II / biosynthesis,  metabolism
Nitriles / pharmacology
Signal Transduction
Skin / cytology
Sulfones / pharmacology
Tumor Necrosis Factor-alpha / antagonists & inhibitors,  immunology,  metabolism
Grant Support
ID/Acronym/Agency:
CA 11623/CA/NCI NIH HHS; CA 49062/CA/NCI NIH HHS; ES 12888/ES/NIEHS NIH HHS; P01 CA049062/CA/NCI NIH HHS; P41 RR011623/RR/NCRR NIH HHS; R01 ES012888/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/3-(4-methylphenylsulfonyl)-2-propenenitrile; 0/Antibodies, Monoclonal; 0/Benzoates; 0/DNA, Mitochondrial; 0/Imidazoles; 0/NF-kappa B; 0/Nitriles; 0/Sulfones; 0/Tumor Necrosis Factor-alpha; 145757-47-7/1,3-dihydroxy-4,4,5,5-tetramethyl-2-(4-carboxyphenyl)tetrahydroimidazole; EC 1.14.13.39/NOS2 protein, human; EC 1.14.13.39/Nitric Oxide Synthase Type II; EC 1.14.99.1/Cyclooxygenase 2; EC 2.4.2.8/Hypoxanthine Phosphoribosyltransferase
Comments/Corrections

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