Document Detail


Differential impact of mouse Rad9 deletion on ionizing radiation-induced bystander effects.
MedLine Citation:
PMID:  16238443     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The cellular response to ionizing radiation is not limited to cells irradiated directly but can be demonstrated in neighboring "bystander" populations. The ability of mouse embryonic stem (ES) cells to express a bystander effect and the role of the radioresistance gene Rad9 were tested. Mouse ES cells differing in Rad9 status were exposed to broad-beam 125 keV/ microm 3He alpha particles. All populations, when confluent, demonstrated a dose-independent bystander effect with respect to cell killing, and the Rad9-/- genotype did not selectively alter that response or cell killing after direct exposure to this high-LET radiation. In contrast, relative to Rad9+/+ cells, the homozygous mutant was sensitive to direct exposure to alpha particles when in log phase, providing evidence of a role for Rad9 in repair of potentially lethal damage. Direct exposure to alpha particles induced an increase in the frequency of apoptosis and micronucleus formation, regardless of Rad9 status, although the null mutant showed high spontaneous levels of both end points. All populations demonstrated alpha-particle-induced bystander apoptosis, but that effect was most prominent in Rad9-/- cells. Minimal alpha-particle induction of micronuclei in bystander cells was observed, except for the Rad9-/- mutant, where a significant increase above background was detected. Therefore, the Rad9 null mutation selectively sensitizes mouse ES cells to spontaneous and high-LET radiation-induced bystander apoptosis and micronucleus formation, but it has much less impact on cell killing by direct or bystander alpha-particle exposure. Results are presented in the context of defining the function of Rad9 in the cellular response to radiation and its differential effects on individual bystander end points.
Authors:
Aiping Zhu; Hongning Zhou; Corinne Leloup; Stephen A Marino; Charles R Geard; Tom K Hei; Howard B Lieberman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Radiation research     Volume:  164     ISSN:  0033-7587     ISO Abbreviation:  Radiat. Res.     Publication Date:  2005 Nov 
Date Detail:
Created Date:  2005-10-21     Completed Date:  2005-12-28     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0401245     Medline TA:  Radiat Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  655-61     Citation Subset:  IM; S    
Affiliation:
Center for Radiological Research, Columbia University College of Physicians and Surgeons, New York, New York 10032, USA.
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MeSH Terms
Descriptor/Qualifier:
Alpha Particles
Animals
Apoptosis / radiation effects
Bystander Effect / radiation effects*
Cell Cycle Proteins / physiology*
DNA Damage
Mice
Micronuclei, Chromosome-Defective / radiation effects
Grant Support
ID/Acronym/Agency:
CA49062/CA/NCI NIH HHS; CA75061/CA/NCI NIH HHS; CA89816/CA/NCI NIH HHS; EB002033/EB/NIBIB NIH HHS; ES12888/ES/NIEHS NIH HHS; GM52493/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 139691-42-2/rad9 protein

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