Vitamin D Receptor Regulation of the Steroid/Bile Acid Sulfotransferase SULT2A1

Chatterjee, Bandana; Echchgadda, Ibtissam; Song, Chung S.

doi:10.1016/s0076-6879(05)00010-8

Cited by 70 publications

(48 citation statements)

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“…The relative levels of Sult2A1 mRNAs in the hormone-injected and control mice were determined from the linear range of the standard curve and fold induction was calculated. The RT-PCR data is in line with our earlier Northern blot results, which showed 3.8 to 6-fold induction of Sult2A1 mRNAs in D 3 -injected mice (Chatterjee et al, 2005;Song et al, 2006). Animal-to animal variation can explain the 3-to 6-fold induction range.…”

Section: Induction Of Sult2a1 Mrnas and The Ir0 Enhancer In The Mousesupporting

confidence: 91%

“…The enzyme is expressed at high abundance in the first-pass tissues (liver and intestine) and in the steroidogenic tissue of the adrenal gland. Multiple nuclear receptors including PXR, CAR and VDR can induce SULT2A1 in cultured cells and in vivo in the mouse liver (Song et al, 2001;Sonoda et al, 2002;Echchgadda et al, 2004a;Assem et al, 2004;Maglich et al, 2004;Fang et al, 2005;Seeley et al, 2005;Chatterjee et al, 2005;Song et al, 2006). We had shown earlier that the vitamin D 3 -and xenobiotic-mediated induction of the mouse Sult2A1 promoter in transfected liver and intestinal cells is dependent upon binding of the corresponding receptors to a 21-base pair inverted repeat (IR0) enhancer (Echchgadda et al, 2004b).…”

Section: Introductionmentioning

confidence: 99%

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Xenobiotic- and vitamin D-responsive induction of the steroid/bile acid-sulfotransferase Sult2A1 in young and old mice: The role of a gene enhancer in the liver chromatin

Seo

Chung

Kim

et al. 2007

Gene

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The xenobiotic-activated nuclear receptors PXR (pregnane X receptor) and CAR (constitutive androstane receptor) and the vitamin D 3 -activated nuclear receptor VDR regulate steroid and xenobiotic metabolism by inducing the phase I cytochrome P450 monooxygenases, phase II conjugating transferases, and the phase III transporters, which mediate the efflux of water-soluble lipid metabolites from cells. Metabolic stress due to the deviant expression of steroid-and xenobioticmetabolizing enzymes is known to have severe health consequences including accelerated aging, and increased expression of these enzymes is associated with extended longevity (Gachon et al, 2006;McElwee et al, 2004). Information on the similarities and dissimilarities in drug metabolism between the young and old, as may be uncovered by studying aging regulation of the genes relevant to steroid and xenobiotic metabolism, is likely to have clinical significance. In this report, we examined the VDR-and PXR-mediated gene induction of the phase II sulfotransferase Sult2A1 in the livers of 4-month and 20-month old mice. Sult2A1 converts bile acids, steroids and a number of drugs to the corresponding sulfated metabolites, which are readily eliminated from the body due to increased water solubility. In RT-PCR assay, aging did not change the induction of Sult2A1 mRNAs by the hormonally active vitamin D 3 and the catatoxic synthetic steroid PCN (pregnenolone-16α-carbonitrile). Chromatin immunoprecipitation (ChIP) from liver nuclei showed that aging had no effect on the activity of an IR0 enhancer in the Sult2A1 chromatin to recruit VDR, RXR-α (retinoid X receptor) and PXR in mice injected with D 3 or PCN. Thus, mice in late life are as competent as those in early life in responding to the hormonal and xenobiotic signaling for Sult2A1 induction. This is the first report describing the role of aging in the functional response of an enhancer in the liver chromatin to the nuclear receptor-dependent signaling.

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Section: Induction Of Sult2a1 Mrnas and The Ir0 Enhancer In The Mousesupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Xenobiotic- and vitamin D-responsive induction of the steroid/bile acid-sulfotransferase Sult2A1 in young and old mice: The role of a gene enhancer in the liver chromatin

Seo

Chung

Kim

et al. 2007

Gene

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“…Activation of VDR by 1a,25-dihydroxyvitamin D 3 induces CYP3A4, CYP2B, and CYP2C in intestinal cells, suggesting a role for VDR in drug and bile acid metabolism (Schmiedlin-Ren et al, 2001). Activation of VDR also induced SULT2A1 and thus simultaneously stimulated bile acid sulfation (Chatterjee et al, 2005). Furthermore, two bile acid transporters (MRP3 and ASBT) were shown to be VDR targets in the intestine Chen et al, 2006).…”

Section: Bile Acid Receptor Signaling In Liver Metabolismmentioning

confidence: 96%

Bile Acid Signaling in Metabolic Disease and Drug Therapy

2014

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“…8, an increase associated with enhanced responsiveness of the cells to 1,25(OH) 2 D 3 (Liel et al 1992). Increased VDR expression as a result of E2 treatment has also been noted in other tissues and cell types, such as the uterus (Levy et al 1984), liver (Chatterjee et al 2005), and human breast cancer cells (Escaleira et al 1993, Gilad et al 2005. However, E2 has also been associated with enhanced breast and uterus carcinogenesis.…”

Section: Introductionmentioning

confidence: 95%

Phytoestrogens regulate transcription and translation of vitamin D receptor in colon cancer cells

Gilad¹,

Tirosh²,

Schwartz³

2006

Journal of Endocrinology

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The present study assesses the effects of two isoflavones, genistein and glycitein, and equol -a product of intestinal bacterial metabolism of dietary isoflavones, on vitamin D receptor (VDR) expression in an intestinal HT29 cell line. Genistein and glycitein significantly upregulated the VDR transcription and translation in HT29 cells. The effect of equol was less pronounced.Treating HT29 cells transfected with a vector containing the VDR promoter next to a luciferase reporter with genistein or glycitein resulted in significant upregulation of VDR promoter activity, in a manner similar to that induced by 17b-estradiol (E2). Again, the effect of equol was less pronounced. VDR luciferase promoter activity was upregulated most by genistein, then by glycitein and least by equol when the VDR promoter was cotransfected with estrogen receptor b.Reporter gene and chromatin immunoprecipitation (ChIP) assays demonstrated that E2 upregulates AP-1 and Sp-1 sites present on the VDR gene. In contrast, the same assays demonstrated that the Sp-1, but not AP-1, site is induced by the phytoestrogens.Similar to E2, genistein, glycitein and the isoflavonoid metabolite equol induced higher concentrations of intracellular free calcium, an event that could provide the upstream mechanism(s) induced by E2 and phytoestrogens that initiates the signaling cascade which results in the activation of extracellular signal-regulated kinase (ERK) signaling pathways and modulation of Sp-1 sites of the VDR gene, and culminates in enhanced VDR expression.

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Vitamin D Receptor Regulation of the Steroid/Bile Acid Sulfotransferase SULT2A1

Cited by 70 publications

References 50 publications

Xenobiotic- and vitamin D-responsive induction of the steroid/bile acid-sulfotransferase Sult2A1 in young and old mice: The role of a gene enhancer in the liver chromatin

Xenobiotic- and vitamin D-responsive induction of the steroid/bile acid-sulfotransferase Sult2A1 in young and old mice: The role of a gene enhancer in the liver chromatin

Bile Acid Signaling in Metabolic Disease and Drug Therapy

Phytoestrogens regulate transcription and translation of vitamin D receptor in colon cancer cells

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