Differential Effects of Interleukin-1β, Interleukin-2, and Interferon-γ on the Inducible Expression of CYP 1A1 and CYP 1A2 in Cultured Rabbit Hepatocytes

Calleja, Cécile; Eeckhoutte, C.; Larrieu, G.; Dupuy, Jacques; Pineau, Thierry; Galtier, P.

doi:10.1006/bbrc.1997.7468

Cited by 24 publications

(12 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It could conceivably be related to putative modulation by TCDD/AhR on other modes of signaling that are known to be able to suppress CYP1A1 expression (e.g., see Refs. [65][66][67]. Because CYP1A1 is known to be up-regulated in rat prostate by TCDD exposure (68,69), the apparent inconsistency that our data present may be due to inherent differences in context afforded by CaP cell lines versus normal prostate epithelia in vivo.…”

Section: Discussionmentioning

confidence: 61%

Identification of Aryl Hydrocarbon Receptor as a Putative Wnt/β-Catenin Pathway Target Gene in Prostate Cancer Cells

Chesire¹,

Dunn²,

Ewing³

et al. 2004

Cancer Research

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 61%

Identification of Aryl Hydrocarbon Receptor as a Putative Wnt/β-Catenin Pathway Target Gene in Prostate Cancer Cells

Chesire¹,

Dunn²,

Ewing³

et al. 2004

Cancer Research

View full text Add to dashboard Cite

show abstract

“…On the other hand, it has been reported that both TNF and IL-6 decrease the expression of mRNA for CYP isozymes [24][25][26] . These findings suggest that one of the mechanisms of reduced mRNA expression of CYP isozymes in obstructive jaundice may an increase in the level of cytokines such as TNF and IL-6.…”

Section: Discussionmentioning

confidence: 99%

Effect of biliary obstruction and internal biliary drainage on hepatic cytochrome P450 isozymes in rats

Fukushima¹,

Okuno²,

Shibatani³

et al. 2008

WJG

View full text Add to dashboard Cite

AIM:To investigate the total cytochrome P450 (CYP) content, microsomal mixed-function oxidase (MFO) activity, and expression of mRNAs for various CYP isozymes in a simple rat model of reversible obstructive jaundice. METHODS:Obstructive jaundice was created in male rats by causing bile duct obstruction with polyester tape. In another group of rats, bile duct obstruction was followed by internal biliary drainage after releasing the tape. The expression of various CYP isozyme mRNAs was semi-quantitatively assessed by competitive RT-PCR. RESULTS:The total CYP content and microsomal MFO activity showed a significant decrease after biliary obstruction, but returned to respective control levels after biliary drainage. A marked reduction in the expression of CYP1A2, 2B1/2, 2C11, 2E1, 3A1, and 3A2 mRNA was detected during biliary obstruction, while expression increased significantly toward the control level after biliary drainage. Although expression of CYP4A1 mRNA showed no reduction during biliary obstruction, it still increased significantly after biliary drainage. CONCLUSION:These results suggest that not only obstructive jaundice, but also the subsequent internal biliary drainage may affect regulatory medications of the synthesis of individual CYP isozymes differently.

show abstract

“…6b). Finally, several cytokines such as interleukin-1␤, tumor necrosis factor, and interferon-␥ are reported to inhibit induced expression of CYP1A1 and CYP1A2 genes (33,34). Since NF-B is known to work as a downstream effector of these cytokines (35), the inhibitions of cytochrome P450 induction could be explained through the enhanced synthesis of AhRR by NF-B.…”

Section: Discussionmentioning

confidence: 99%

Structure and Expression of the Ah Receptor Repressor Gene

Baba¹,

Mimura²,

Gradin³

et al. 2001

Journal of Biological Chemistry

156

105

View full text Add to dashboard Cite

The aryl hydrocarbon receptor (AhR) repressor (AhRR) gene has been isolated and characterized from a mouse genomic library. The gene is distributed as 11 exons in a total length of about 60 kilobase pairs. Fluorescence in situ hybridization analysis has shown that the AhRR gene is located at mouse chromosome 13C2, at rat chromosome 1p11.2, and at human chromosome 5p15.3. The AhRR gene has a TATA-less promoter and several transcription start sites. In addition, putative regulatory DNA sequences such as xenobiotic responsive element (XRE), GC box, and NF-B-binding sites have been identified in the 5-upstream region of the AhRR gene. Transient transfection analyses of HeLa cells with reporter genes that contain deletions and point mutations in the AhRR promoter revealed that all three XREs mediated the inducible expression of the AhRR gene by 3-methylcholanthrene treatment, and furthermore, GC box sequences were indispensable for a high level of inducible expression and for constitutive expression. Moreover, by using gel mobility shift assays we were able to show that the AhR/Arnt heterodimer binds to the XREs with very low affinity, which is due to three varied nucleotides outside the XRE core sequence. We have also shown that Sp1 and Sp3 can bind to the GC boxes. Finally, both transient transfection analysis and gel mobility shift assay revealed that the AhRR gene is up-regulated by a p65/p50 heterodimer that binds to the NF-B site when the cells has been exposed to 12-O-tetradecanoylphorbol-13-acetate, and this inducible expression was further enhanced by cotreatment of 12-O-tetradecanoylphorbol-13-acetate and 3-methylcholanthrene.

show abstract

Differential Effects of Interleukin-1β, Interleukin-2, and Interferon-γ on the Inducible Expression of CYP 1A1 and CYP 1A2 in Cultured Rabbit Hepatocytes

Cited by 24 publications

References 0 publications

Identification of Aryl Hydrocarbon Receptor as a Putative Wnt/β-Catenin Pathway Target Gene in Prostate Cancer Cells

Identification of Aryl Hydrocarbon Receptor as a Putative Wnt/β-Catenin Pathway Target Gene in Prostate Cancer Cells

Effect of biliary obstruction and internal biliary drainage on hepatic cytochrome P450 isozymes in rats

Structure and Expression of the Ah Receptor Repressor Gene

Contact Info

Product

Resources

About