Gene-Selective Histone H3 Acetylation in the Absence of Increase in Global Histone Acetylation in Liver of Rats Chronically Fed Alcohol

Title
Gene-Selective Histone H3 Acetylation in the Absence of Increase in Global Histone Acetylation in Liver of Rats Chronically Fed Alcohol
Author(s)
박필훈로버트 림[로버트 림]슈벤드라 슈클라[슈벤드라 슈클라]
Keywords
ACETYLTRANSFERASE P300; FATTY LIVER; ETHANOL; EXPRESSION; DEHYDROGENASE; INJURY; DEACETYLASES; HEPATOCYTES; ACTIVATION; INHIBITORS
Issue Date
201205
Publisher
OXFORD UNIV PRESS
Citation
ALCOHOL AND ALCOHOLISM, v.47, no.3, pp.233 - 239
Abstract
Aims: The aim of this study was to determine the effect of chronic ethanol feeding on acetylation of histone H3 at lysine 9 (H3-Lys9) at promoter and coding regions of genes for class I alcohol dehydrogenase (ADH I), inducible nitric oxide synthase (iNOS), Bax, p21, c-met and hepatocyte growth factor in the rat liver. Methods: Rats were fed ethanol-containing liquid diet (5%, w/v) for 1-4 weeks. The global level of acetylation of H3-Lys9 in the liver was examined by western blot analysis. The levels of mRNA for various genes were measured by real-time reverse transcriptase-polymerase chain reaction. The association of acetylated histone H3-Lys9 with the different regions of genes was monitored by chromatin immunoprecipitation assay. Results: Chronic ethanol treatment increased mRNA expression of genes for iNOS, c-jun and ADH 1. Chronic ethanol treatment did not cause increase in global acetylation of H3-Lys9, but significantly increased the association of acetylated histone H3-Lys9 in the ADH I gene, both in promoter and in coding regions. In contrast, chronic ethanol treatment did not significantly increase the association of acetylated histone H3-Lys9 with iNOS and c-jun genes. Conclusion: Chronic ethanol exposure increased the gene-selective association of acetylated H3-Lys9 in the absence of global histone acetylation. Thus, not all genes expressed by ethanol are linked to transcription via histone H3 acetylation at Lys9.
URI
http://hdl.handle.net/YU.REPOSITORY/28386http://dx.doi.org/10.1093/alcalc/ags004
ISSN
0735-0414
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약학대학 > 약학부 > Articles
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