Document Detail


Cell cycle regulators modulating con A mitogenesis and apoptosis in low-dose radiation-exposed mice.
MedLine Citation:
PMID:  15715507     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Low doses of ionizing radiation (LDR) are reported to induce transient changes in mouse lymphocytes, such as enhanced response to polyclonal T cell mitogens, increased expression of heat shock proteins, and p53. We evaluated the role of cell cycle proteins and apoptosis in lymphocytes of C57BL/6 mice exposed to 20 cGy fractionated LDR. We found an enhanced cell proliferation in response to the mitogen concanavalin A (con A). The expression of several cell cycle and apoptosis-related intracellular and extracellular proteins was analyzed by flowcytometry following labeling with specific antibodies. An increased response to con A was accompanied by an increase in the expression of proliferating cell nuclear antigen (PCNA) and cyclins D and A. The expression of cyclin B did not change significantly. In 20 cGy-exposed C57BL/6 mice, the caspase activity and apoptosis were reduced in con A-stimulated spleen cells as compared to sham controls. The expression of Fas and Fas ligand was analyzed by labeling with specific antibodies followed by flowcytometry. There was no change in the expression of Fas and Fas ligand. The change in the mitochondrial transmembrane potential was followed by labeling the cells with the dye 5,5',6,6',-tetrachloro-1,1,3,3-tetraethylbenzimidazolcarbocyanine iodide (JC-I) and analyzing by flowcytometry. Mitochondrial stability was increased in spleen cells of LDR-treated mice. These data suggest that LDR induces augmentation of mitogenic response by modulation of expression of cyclins and the mitochondrial membrane potential leading to reduced apoptosis.
Authors:
Bhavani Shankar; Krishna B Sainis
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer     Volume:  24     ISSN:  0731-8898     ISO Abbreviation:  J. Environ. Pathol. Toxicol. Oncol.     Publication Date:  2005  
Date Detail:
Created Date:  2005-02-17     Completed Date:  2005-03-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8501420     Medline TA:  J Environ Pathol Toxicol Oncol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  33-43     Citation Subset:  IM    
Affiliation:
Immunology Section, Radiation Biology Health Sciences Division, Bhabha Atomic Research Centre, Modular Laboratories, Trombay, Mumbai, India.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / drug effects,  radiation effects*
Caspases / metabolism
Cell Cycle
Cell Cycle Proteins / physiology*
Cell Proliferation / drug effects,  radiation effects*
Cells, Cultured
Concanavalin A / pharmacology
Cyclin A / metabolism
Cyclin B / metabolism
Cyclin D1 / metabolism
Fas Ligand Protein
Female
Gamma Rays
Intracellular Membranes / radiation effects
Membrane Glycoproteins / metabolism
Membrane Potentials
Mice
Mice, Inbred C57BL
Proliferating Cell Nuclear Antigen / metabolism
Spleen / metabolism,  radiation effects
T-Lymphocytes / radiation effects*
Whole-Body Irradiation
Chemical
Reg. No./Substance:
0/Cell Cycle Proteins; 0/Cyclin A; 0/Cyclin B; 0/Fas Ligand Protein; 0/Fasl protein, mouse; 0/Membrane Glycoproteins; 0/Proliferating Cell Nuclear Antigen; 11028-71-0/Concanavalin A; 136601-57-5/Cyclin D1; EC 3.4.22.-/Caspases

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