NDLI: The induction of the human hepatic CYP2E1 gene by interleukin 4 is transcriptional and regulated by protein kinase C

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The effect of the trichloroethylene metabolites trichloroacetate and dichloroacetate on peroxisome proliferation and DNA synthesis in cultured human hepatocytes

Cell Biology and Toxicology : Volume 16, Issue 3, June 2000

Cell Biology and Toxicology : Volume 16, Issue 2, April 2000

Cell Biology and Toxicology : Volume 16, Issue 1, February 2000

Cell Biology and Toxicology : Volume 15

Cell Biology and Toxicology : Volume 14

Cell Biology and Toxicology : Volume 13

The induction of the human hepatic CYP2E1 gene by interleukin 4 is transcriptional and regulated by protein kinase C

Content Provider	Springer Nature Link
Author	Lagadic Gossmann, D. Lerche, C. Rissel, M. Joannard, F. Galisteo, M. Guillouzo, A. Corcos, L.
Copyright Year	2000
Abstract	Cytochrome P4502E1 (CYP2E1) plays a key role in the metabolism of numerous drug substrates, mostly in mammalian liver. Both the apoprotein and mRNA levels are increased in response to interleukin 4 (IL-4) in primary human hepatocyte cultures. We developed a human hepatoma cell model that faithfully reproduces the responsiveness of the CYP2E1 gene to IL-4 at least in part through transcriptional activation, upon treatment with 150 U/ml of IL-4. As expected, IL-4 induced tyrosine phosphorylation of the STAT6 transcription factor, an effect prevented by the tyrosine kinase inhibitor tyrphostin A25. However, this inhibitor as well as genistein (another inhibitor of tyrosine kinases) had no effect on the IL-4 induction of CYP2E1. Similarly, protein kinase A activators (forskolin and dibutyryl-cAMP) and inhibitor (H89) did not influence the response to IL-4. However, PKC inhibitors (H7 and calphostin C) strongly blocked any induction of the gene, as well as the IL-4-dependent translocation of PKCζ. Taken together, our results show that IL-4 coordinately induces CYP2E1 transcription, mRNA and apoprotein levels in human hepatoma cells in a PKC-dependent manner, potentially through the activity of the PKCζ isoform.
Starting Page	221
Ending Page	233
Page Count	13
File Format	PDF
ISSN	07422091
Journal	Cell Biology and Toxicology
Volume Number	16
Issue Number	4
e-ISSN	15736822
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2000-01-01
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Pharmacology/Toxicology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Health, Toxicology and Mutagenesis Toxicology

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