Regulation of sulfotransferase gene expression by glucocorticoid hormones and xenobiotics in primary rat hepatocyte culture

Runge‐Morris, Melissa

doi:10.1016/s0009-2797(97)00142-7

Cited by 51 publications

(49 citation statements)

References 23 publications

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“…Genes encoding different SULT isoforms expression can be regulated through endogenous hormones (growth hormone, sex hormones, thyroid hormones, glucocorticoids) and immune system (cytokines) in different ways and at various levels, being also tissue-dependent (Liu and Klaassen, 1996;Duanmu et al, 2001;Dunn and Klaassen, 2000;Klaassen et al, 1998;Runge-Morris, 1998;RungeMorris et al, 1999;Wu et al, 2001;Runge-Morris and Kocarek, 2005;Chen et al, 2008;Maiti and Chen, 2003a;2003b). Glucocorticoid-inducible rat hepatic SULT1A1 gene transcription occurs through a Glucocorticoid Receptor (GR)-mediated mechanism, a low dose of a synthetic glucocorticoid, can have physiologically significant effects attributable to the increased expression of SULT1A1 (Runge-Morris and Kocarek, 2005).…”

Section: Discussionmentioning

confidence: 99%

“…Treatment of human hepatocyte cultures with PXRactivating concentrations of dexamethasone and rifampicin both produced concentration-dependent increases in human SULT2A1 mRNA and protein contents (Fang et al, 2005a;2005b;Duanmu et al, 2002). In addition, more and more recent data suggest that hepatic SULT gene expression is regulated by the same transcription factor networks that also control the expression of the Cytochrome P450s (CYP), such as the Aryl hydrocarbon (Ah) receptor and members of the nuclear receptor superfamily, such as PXR, CAR and PPARα, although the co-regulation between the SULT and CYP gene families doesn't always occur in a coordinate direction (Runge-Morris, 1998;Runge-Morris and Kocarek, 2005;Jain et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

“…Xenobiotic induction of SULTs is not well studied. Recent data suggest that SULTs can be induced by xenobiotics, although the mechanisms for xenobiotic induction are less known (Runge-Morris and Kocarek, 2005;1998;Chen et al, 2008;Maiti and Chen, 2003a;2003b). Psychostimulants regulation of SULTs is basically not studied.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Methamphetamine Regulation of Sulfotransferases in Rat Liver and Brain

Zhou¹

2010

American Journal of Pharmacology and Toxicology

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Problem statement: Sulfotransferases (SULTs) are important phase II drug metabolizing enzymes. They also regulate the biological activities of various hormones. To the best of our knowledge, psychostimulants regulation of SULTs is basically not studied except one article reported that Methamphetamine (METH) treatment induced rat amygdale rSULT1A1 mRNA 4.3 fold by using microarray method to identify a series of candidate genes after single-dose METH treatment. The psychostimulant METH is used to treat disorders such as attention deficit, narcolepsy and obesity. It is also a highly addictive drug that causes serious social problems. The abuse of this drug leads to the damage of monoaminergic systems in the mammalian brain. It is important to understand how SULT expressions are regulated by psychostimulants. Approach: This study was performed to evaluate the effect of METH on SULT gene expressions in rat liver and brain. METH (0, 1, 5, 20 mg kg −1 day −1 ) was used to treat male and female rats for 7 days by oral administration. Rat livers and brains were collected 24 h after the final drug treatment. Western blot and real-time RT-PCR were used to investigate the effect of METH on SULT protein and mRNA expression, respectively, in rat liver and brain. Results: Proteins and mRNAs of rSULT1A1, rSULT2A1 and rSULT1E1 were induced in liver and brain of both male and female rats following METH treatment. rSULT1E1 was induced at much higher level compared to that of rSULT1A1 and rSULT2A1. Brain inductions were found to be much higher than those found in liver. Conclusion: These data suggest an important role of the central dopaminergic system in the regulation of liver and brain rSULT expressions.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Methamphetamine Regulation of Sulfotransferases in Rat Liver and Brain

Zhou¹

2010

American Journal of Pharmacology and Toxicology

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“…9). PXR ligands have been reported to induce the expression of Sult1a1 in female rats (Hartley et al, 2004), male rats (Liu and Klaassen, 1996;Rushmore and Kong, 2002), 1b1 in female rats (Hartley et al, 2004); 1d1 and 1e1 in male mice (Sonoda et al, 2002); 2a1 in male rats (Liu and Klaassen, 1996;Runge-Morris et al, 1996;Rushmore and Kong, 2002), male mice (Sonoda et al, 2002;Echchgadda et al, 2004a;Kim et al, 2004), female mice (Sonoda et al, 2002), and human hepatocytes (Duanmu et al, 2002); and PAPSs2 in male mice (Sonoda et al, 2002). In contrast, PXR ligands were reported to have no influence on the expression of Sult1a1 in male mice (Maglich et al, 2002), human hepatocytes (Duanmu et al, 2002), male rats (Liu and Klaassen, 1996;Duanmu et al, 2001), and female rats (Liu and Klaassen, 1996); 1c1 in male and female rats (Liu and Klaassen, 1996); 1d1 in male mice (Maglich et al, 2002); 1e1 in male and female rats (Liu and Klaassen, 1996); 2a1 in mice (Saini et al, 2004), and male and female rats (Liu and Klaassen, 1996); and 2b1 in male mice (Maglich et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Regulation of Sulfotransferase Enzymes by Prototypical Microsomal Enzyme Inducers in Mice

Alnouti

Klaassen

2007

J Pharmacol Exp Ther

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“…Previously, the effects of glucocorticoid hormones on rat hepatic aryl sulfotransferase IV gene expression were investigated in primary rat hepatocyte cultures and show that the expression is up-regulated by glucocorticoids. 49 Analogues of clofibrate (fibrates), which are hypolipidemic in humans and rodents, induce a variety of hepatic changes when administered to rats in vivo, including proliferation of peroxisomes and induction of several peroxisomal enzymes in liver, including carnitine acetyltransferase, catalase, and enoyl-CoA hydratase. We tested at both the light-and electron-microscopy level whether the TD hepatocytes could also respond to ciprofibrate and increase the cellular content of catalase.…”

Section: Discussionmentioning

confidence: 99%

Differentiated properties of hepatocytes induced from pancreatic cells

2002

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Transdifferentiation of pancreas to liver is a well-recognized phenomenon and has been described in animal experiments and human pathology. We recently produced an in vitro model for the transdifferentiation (or conversion) of the pancreatic cell line AR42J-B13 to hepatocytes based on culture with dexamethasone (Dex). To determine whether the hepatocytes express markers of hepatic intermediary metabolism and detoxification, we investigated the patterns of expression of glucokinase, cytochrome P450s CYP3A1 and CYP2B1/2, testosterone/4-nitrophenol uridine diphosphate glucuronosyltransferase (UDPGT), and aryl sulfotransferase. All were expressed. We also determined the expression of 2 enzymes involved in ammonia detoxification: carbamoylphosphate synthetase I (CPS I) and glutamine synthetase (GS). These enzymes are normally strictly compartmentalized in liver in a wide periportal pattern and the last downstream perivenous hepatocytes, respectively. Following culture with Dex, CPS I and GS are expressed in 2 different cell populations, suggesting that both periportal and perivenous hepatocytes are induced. We also produced a reporter assay based on the activation of green fluorescent protein (GFP) by the transthyretin (TTR) promoter or glucose-6-phosphatase (G6Pase) promoter. After culture with Dex, transfected cells begin to express GFP, showing that hepatic promoters are activated in concert with the induction of the hepatocyte phenotype. Lastly, we examined the stability of the hepatic phenotype and found that some cells still express liver markers (transferrin or albumin) up to 14 days after removal of Dex. In conclusion, these results suggest that pancreatic hepatocytes produced by this method may offer an alternative model to primary cultures of hepatocytes for the study of liver function. (HEPATOLOGY 2002;36:534-543.) I n vitro cultures of hepatocytes offer a valuable tool in the investigation of liver function. However, the major limitation to the use of cultured hepatocytes is their rapid loss of differentiated properties and gain of a more fetal/neoplastic phenotype. 1-3 For example, the loss of differentiated phenotype is most apparent in the rapid decline of total cytochrome P450 (CYP) after isolation and in culture, particularly the CYP3A1 isoform. 2 Dedifferentiation is reflected not only in decreased liver-specific functions but also in an alteration of morphology; the cells flatten, depolarize, and lose many of the surface characteristics of normal hepatocytes in vivo. The mechanisms responsible for loss of differentiated properties include down-regulation of transcription factors (e.g., C/EBP␣ and HNF1) involved in liver-specific gene expression and a switch from a quiescent to a proliferative mode. 2 It is also difficult to examine the long-term effects of exogenous factors on hepatic gene expression and liver function. Culture conditions that maintain primary rat hepatocytes in a highly differentiated state have recently been developed, but these still have selective expression of hepatic marke...

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Regulation of sulfotransferase gene expression by glucocorticoid hormones and xenobiotics in primary rat hepatocyte culture

Cited by 51 publications

References 23 publications

Methamphetamine Regulation of Sulfotransferases in Rat Liver and Brain

Methamphetamine Regulation of Sulfotransferases in Rat Liver and Brain

Regulation of Sulfotransferase Enzymes by Prototypical Microsomal Enzyme Inducers in Mice

Differentiated properties of hepatocytes induced from pancreatic cells

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