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All-trans retinoic acid inhibits the recruitment of ARNT to DNA, resulting in the decrease of CYP1A1 mRNA expression in HepG2 cells
Title: | All-trans retinoic acid inhibits the recruitment of ARNT to DNA, resulting in the decrease of CYP1A1 mRNA expression in HepG2 cells |
Authors: | Ohno, Marumi Browse this author | Ikenaka, Yoshinori Browse this author →KAKEN DB | Ishizuka, Mayumi Browse this author →KAKEN DB |
Keywords: | Retinoic acid | Aryl hydrocarbon receptor | Aryl hydrocarbon receptor nuclear translocator | Recruitment |
Issue Date: | 6-Jan-2012 |
Publisher: | Elsevier |
Journal Title: | Biochemical and Biophysical Research Communications |
Volume: | 417 |
Issue: | 1 |
Start Page: | 484 |
End Page: | 489 |
Publisher DOI: | 10.1016/j.bbrc.2011.11.146 |
PMID: | 22177959 |
Abstract: | Aryl hydrocarbon receptor (AHR) and AHR nuclear translocator (ARNT) are well-conserved transcription factors among species. However, there are a very limited number of reports on the physiological function of AHR, particularly on the regulation of AHR by endogenous compounds. We hence investigated the effects of all-trans retinoic acid (atRA) on cytochrome P450 (CYP)1A1 gene transcription as a model of AHR-regulated transcription mechanisms in HepG2 cells, a human hepatoma cell line. Treatment with atRA significantly reduced transactivation and expression of CYP1A1 mRNA to less than half of its control value, and this inhibitory effect was mediated by RARα. The result of chromatin immunoprecipitation assay indicated that treatment with atRA at 1-100 nM drastically inhibited the recruitment of ARNT to DNA regions containing xenobiotic responsive elements. In conclusion, atRA at physiological concentrations could reduce AHR-mediated gene transcription via the inhibition of recruitment of ARNT to relevant DNA regions. |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/48497 |
Appears in Collections: | 獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 石塚 真由美
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