Regulation of CYP1A2 by histone deacetylase inhibitors in mouse hepatocytes

Journal of Biochemical and Molecular Toxicology
Bohwan Jin, Doug-Young Ryu

Abstract

Cytochrome P450 1A2 (CYP1A2) is constitutively expressed in the mouse liver, but the constitutive expression progressively declines to an undetectable level in isolated hepatocytes. In this study, CYP1A2 was induced in hepatocytes exposed to the histone deacetylase inhibitors trichostatin A (TSA) and sodium butyrate (SB), but only well after constitutive CYP1A2 expression was silenced. However, cotreatment with the arylhydrocarbon receptor (AhR) ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and either TSA or SB reduced the induction of CYP1A2 with the same time course as TSA or SB increased its induction. These results suggest that histone modification is involved in CYP1A2 regulation in hepatocytes through pathways that are independent of AhR.

References

Mar 1, 1988·Journal of Cellular Physiology·E G SchuetzP S Guzelian

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Citations

Aug 16, 2005·Toxicology in Vitro : an International Journal Published in Association with BIBRA·Marcella MartignoniMario Monshouwer
Jan 1, 2009·Expert Review of Clinical Pharmacology·Alvin Gomez, Magnus Ingelman-Sundberg
Jan 24, 2021·Archives of Pharmacal Research·Yeo-Jung KwonYoung-Jin Chun

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