Induction of CYP1A1 gene expression in H4-II-E rat hepatoma cells by benzo[e]pyrene

1992 ◽  
Vol 5 (3) ◽  
pp. 232-237 ◽  
Author(s):  
William H. Houser ◽  
Abhijit Raha ◽  
Michelle Vickers
Keyword(s):  
Gene Expression ◽  
Hepatoma Cells ◽  
Cyp1a1 Gene ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

Osmotic Regulation of MAP-Kinase Activities and Gene Expression in H4IIE Rat Hepatoma Cells

1998 ◽  
Vol 379 (6) ◽  
pp. 667-672 ◽  
Author(s):  
Sabine Wiese ◽  
Freimut Schliess ◽  
Dieter Häussinger
Keyword(s):  
Gene Expression ◽  
Map Kinase ◽  
Hepatoma Cells ◽  
Osmotic Regulation ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

Osmotic regulation of betaine homocysteine-S-methyltransferase expression in H4IIE rat hepatoma cells

2007 ◽  
Vol 292 (4) ◽  
pp. G1089-G1098 ◽  
Author(s):  
Christine Schäfer ◽  
Lars Hoffmann ◽  
Katrin Heldt ◽  
Mohammad Reza Lornejad-Schäfer ◽  
Gernot Brauers ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Tyrosine Kinases ◽  
Hepatoma Cells ◽  
Pcr Analysis ◽  
Osmotic Regulation ◽  
A Cell ◽  
Gene Expression Studies ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

Cell hydration changes critically affect liver metabolism and gene expression. In the course of gene expression studies using nylon cDNA-arrays we found that hyperosmolarity (405 mosmol/l) suppressed the betaine-homocysteine methyltransferase ( Bhmt) mRNA expression in H4IIE rat hepatoma cells. This was confirmed by Northern blot and real-time quantitative RT-PCR analysis, which in addition unraveled a pronounced induction of Bhmt mRNA expression by hypoosmotic (205 mosmol/l) swelling. Osmotic regulation of Bhmt mRNA expression was largely paralleled at the levels of Bhmt protein and enzymatic activity. Like hyperosmotic NaCl, hyperosmotic raffinose but not hyperosmotic urea suppressed Bhmt mRNA expression, suggesting that cell shrinkage rather than increased ionic strength or hyperosmolarity per se is the trigger. Hypoosmolarity increased the expression of a reporter gene driven by the entire human BHMT promoter, whereas destabilization of BHMT mRNA was observed under hyperosmotic conditions. Osmosensitivity of Bhmt mRNA expression was impaired by inhibitors of tyrosine kinases and cyclic nucleotide-dependent kinases. The osmotic regulation of BHMT may be part of a cell volume-regulatory response and additionally lead to metabolic alterations that depend on the availability of betaine-derived methyl groups.

scholarly journals Fatty Acids Induce L-CPT I Gene Expression through a PPARα-Independent Mechanism in Rat Hepatoma Cells

2005 ◽  
Vol 135 (10) ◽  
pp. 2313-2319 ◽  
Author(s):  
Cédric Le May ◽  
Michèle Caüzac ◽  
Claire Diradourian ◽  
Dominique Perdereau ◽  
Jean Girard ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Hepatoma Cells ◽  
Independent Mechanism ◽  
Cpt I ◽  
Rat Hepatoma ◽  
I Gene ◽  
Rat Hepatoma Cells

TCDD and PAH-induced CYP1A/B gene expression in H4IIE rat hepatoma cells

2012 ◽  
Vol 211 ◽  
pp. S84
Author(s):  
Sonja Kaisarevic ◽  
Vanja Dakic ◽  
Jelena Hrubik ◽  
Zorana Vujin ◽  
Kristina Pogrmic-Majkic ◽  
...  
Keyword(s):  
Gene Expression ◽  
Hepatoma Cells ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

scholarly journals Transcription factor Nrf2/MafK regulates rat placental glutathione S-transferase gene during hepatocarcinogenesis

2004 ◽  
Vol 380 (2) ◽  
pp. 515-521 ◽  
Author(s):  
Hiromi IKEDA ◽  
Shinzo NISHI ◽  
Masaharu SAKAI
Keyword(s):  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Transcription Factor ◽  
Phase Ii ◽  
Hepatoma Cells ◽  
Carcinoma Cells ◽  
Glutathione S Transferase ◽  
P Gene ◽  
Rat Hepatoma ◽  
Rat Hepatoma Cells

The rat GST-P (placental glutathione S-transferase), a phase II detoxifying enzyme, is not expressed in normal liver cells, but is highly and specifically induced during early hepatocarcinogenesis as well as in hepatocellular carcinoma cells. Results of previous studies indicated that GST-P gene activation was mainly controlled by an enhancer element, GPE1 (GST-P enhancer 1), but the specific activation mechanism of the GST-P gene was not fully understood [Morimura, Suzuki, Hochi, Yuki, Nomura, Kitagawa, Nagatsu, Imagawa and Muramatsu (1993) Proc. Natl. Acad. Sci. U.S.A. 90, 2065–2068; Suzuki, Imagawa, Hirabayashi, Yuki, Hisatake, Nomura, Kitagawa and Muramatsu (1995) Cancer Res. 55, 2651–2655]. In the present study, we investigate the transcription factor Nrf2/MafK heterodimer (where Nrf2 stands for NF-E2 p45-related factor 2) as an activator of the GST-P gene through the action of GPE1 during hepatocarcinogenesis. Electrophoretic mobility-shift assay and footprinting analysis with wild-type GPE1 and GPE1 point mutants showed that the Nrf2/MafK heterodimer specifically bound GPE1. Reporter transfection assays indicated that Nrf2 strongly stimulated GST-P gene expression in mouse F9 embryonal carcinoma cells and H4IIE rat hepatoma cells. Northern-blot analysis indicated that GST-P and Nrf2 mRNA increased in parallel with development of precancerous lesions and hepatocellular carcinoma. Keap1 (Kelch-like ECH-associated protein 1), an inhibitory factor of Nrf2, decreased the activation of GPE1 by Nrf2 and this suppression was restored after treatment with electrophilic compounds. GST-P mRNA expression in H4IIE cells was induced by electrophilic compounds, as was the expression of mRNAs of other phase II detoxifying enzymes. Chromatin immunoprecipitation analyses showed that antibodies both against Nrf2 and against MafK precipitated GPE1 from the chromatin of the pre-neoplastic hepatocytes and rat hepatoma cells (H4IIE and dRLh84), but not from normal hepatocytes. These results indicate that the Nrf2/MafK heterodimer regulates GST-P gene expression during early hepatocarcinogenesis and in hepatoma cells.

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