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Slow elimination of phosphorylated histone {gamma}-H2AX from DNA of terminally differentiated mouse heart cells in situ
Phosphorylation of replacement histone H2AX occurs in megabase chromatin domains around double-strand DNA breaks (DSBs) and this modification (called {gamma}-H2AX) may serve as a useful marker of genome damage and repair in terminally differentiated cells. Here using immunohistochemistry we studied...
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Published in: | Biochemical and biophysical research communications 2006-09, Vol.347 (4) |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
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Summary: | Phosphorylation of replacement histone H2AX occurs in megabase chromatin domains around double-strand DNA breaks (DSBs) and this modification (called {gamma}-H2AX) may serve as a useful marker of genome damage and repair in terminally differentiated cells. Here using immunohistochemistry we studied kinetics of {gamma}-H2AX formation and elimination in the X-irradiated mouse heart and renal epithelial tissues in situ. Unirradiated tissues have 3-5% {gamma}-H2AX-positive cells and in tissues fixed 1 h after X-irradiation {gamma}-H2AX-positive nuclei are induced in a dose-dependent manner approaching 20-30% after 3 Gy of IR. Analysis of mouse tissues at different times after 3 Gy of IR showed that maximal induction of {gamma}-H2AX in heart is observed 20 min after IR and then is decreased slowly with about half remaining 23 h later. In renal epithelium maximum of the {gamma}-H2AX-positive cells is observed 40 min after IR and then decreases to control values in 23 h. This indicates that there are significant variations between non-proliferating mammalian tissues in the initial H2AX phosphorylation rate as well as in the rate of {gamma}-H2AX elimination after X-irradiation, which should be taken into account in the analysis of radiation responses. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2006.07.005 |