Hypoxic inhibition of 3-methylcholanthrene-induced CYP1A1 expression is independent of HIF-1alpha.

Abstract:

:Hypoxia-inducible factor-1alpha (HIF-1alpha) and aryl hydrocarbon receptor (AhR) both require dimerization with AhR nuclear translocator (ARNT) to initiate transcription of their respective target genes. It has been proposed that competition for ARNT results in decreased targeting of AhR to cytochrome P450 1A1 (CYP1A1) under hypoxia. We established primary cultures of HIF-1alpha null hepatocytes to examine the interaction between HIF-1alpha and AhR signaling. Gene expression of known HIF targets phosphoglycerate kinase (PGK), vascular endothelial growth factor (VEGF) and glucose transporter-1 (GLUT-1) increased under hypoxia, but was reduced in the HIF null cultures. Concomitant treatment of cultures with hypoxia (1% O2) and 3-methylcholanthrene (an AhR ligand) did not significantly alter HIF target gene expression. Furthermore, enzymatic activity and transcription of CYP1A1 was inhibited by hypoxia in HIF-1alpha null cultures, indicating that HIF-1alpha is not directly involved in negative regulation of AhR signaling.

journal_name

Toxicol Lett

journal_title

Toxicology letters

authors

Allen JW,Johnson RS,Bhatia SN

doi

10.1016/j.toxlet.2004.09.006

keywords:

subject

Has Abstract

pub_date

2005-01-15 00:00:00

pages

151-9

issue

1

eissn

0378-4274

issn

1879-3169

pii

S0378-4274(04)00435-7

journal_volume

155

pub_type

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