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Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE123804 | GEO | 2018/12/14

REPOSITORIES: GEO

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Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [liver]

Project description:We performed a transcriptomic comparison of the Pxr-regulated genes in the liver and intestine (ileum and colon) using microarrays in adult wild-type (WT) vs Pxr-/- C57Bl6/J male mice treated with the rodent specific Pxr ligand pregnenolone 16α-carbonitrile (PCN) (100 mg/kg i.p. once daily for 4 days).

2018-12-14 | GSE123802 | GEO

Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [ileum]

2018-12-14 | GSE123803 | GEO

Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [colon]

2018-12-18 | GSE123963 | GEO

Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [liver]

Project description:Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [liver]

| PRJNA509892 | ENA

Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine

Project description:Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine

| PRJNA509890 | ENA

Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [colon]

Project description:Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [colon]

| PRJNA510394 | ENA

Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [ileum]

Project description:Comparison of target genes from the pregnane X receptor (Pxr) in the liver vs the intestine [ileum]

| PRJNA509891 | ENA

Pregnenolone-16alpha-carbonitrile inhibits rodent liver fibrogenesis via PXR (pregnane X receptor)-dependent and PXR-independent mechanisms.

Project description:The effect of liver growth stimulation [using the rodent PXR (pregnane X receptor) activator PCN (pregnenolone-16alpha-carbonitrile)] in rats chronically treated with carbon tetrachloride to cause repeated hepatocyte necrosis and liver fibrogenesis was examined. PCN did not inhibit the hepatotoxicity of carbon tetrachloride. However, transdifferentiation of hepatic stellate cells and the extent of fibrosis caused by carbon tetrachloride treatment was significantly inhibited by PCN in vivo. In vitro, PCN directly inhibited hepatic stellate cell transdifferentiation to a profibrogenic phenotype, although the cells did not express the PXR (in contrast with hepatocytes), suggesting that PCN acts independently of the PXR. Mice with a functionally disrupted PXR gene (PXR-/-) did not respond to the antifibrogenic effects of PCN, in contrast with wild-type (PXR+/+) mice, demonstrating an antifibrogenic role for the PXR in vivo. However, PCN inhibited the transdifferentiation of PXR-/--derived mouse hepatic stellate cells in vitro, confirming that there is also a PXR-independent antifibrogenic effect of PCN through a direct interaction with hepatic stellate cells. These data suggest that the PXR is antifibrogenic in rodents in vivo and that a PXR-independent target for PXR activators exists in hepatic stellate cells that also functions to inhibit fibrosis.

| S-EPMC1134989 | biostudies-literature

Pregnane X Receptor (PXR) Polymorphisms and Cancer Treatment.

Project description:Pregnane X Receptor (PXR) belongs to the nuclear receptors' superfamily and mainly functions as a xenobiotic sensor activated by a variety of ligands. PXR is widely expressed in normal and malignant tissues. Drug metabolizing enzymes and transporters are also under PXR's regulation. Antineoplastic agents are of particular interest since cancer patients are characterized by significant intra-variability to treatment response and severe toxicities. Various PXR polymorphisms may alter the function of the protein and are linked with significant effects on the pharmacokinetics of chemotherapeutic agents and clinical outcome variability. The purpose of this review is to summarize the roles of PXR polymorphisms in the metabolism and pharmacokinetics of chemotherapeutic drugs. It is also expected that this review will highlight the importance of PXR polymorphisms in selection of chemotherapy, prediction of adverse effects and personalized medicine.

| S-EPMC8394562 | biostudies-literature

The major human pregnane X receptor (PXR) splice variant, PXR.2, exhibits significantly diminished ligand-activated transcriptional regulation.

Project description:The pregnane X receptor (PXR; PXR.1) can be activated by structurally diverse lipophilic ligands. PXR.2, an alternatively spliced form of PXR, lacks 111 nucleotides encoding 37 amino acids in the ligand binding domain. PXR.2 bound a classic CYP3A4 PXR response element (PXRE) in electrophoretic mobility shift assays, but transfected PXR.2 failed to transactivate a CYP3A4-promoter-luciferase reporter plasmid in HepG2 cells treated with various PXR ligands. Cotransfection experiments showed that PXR.2 behaved as a dominant negative, interfering with PXR.1/rifampin activation of CYP3A4-PXRE-LUC. In HepG2 and LS180 cells stably transduced with PXR.1, PXR target genes (CYP3A4, MDR1, CYP2B6, and UGT1A1) were higher than mock-transduced cells in the absence of ligand and were further induced in the presence of rifampin. In contrast, PXR.2 stably introduced into the same host cells failed to induce target genes over levels in mock-transfected cells after drug treatment. Our homology modeling suggests that ligands bind PXR.1 more favorably, probably because of the presence of a key disordered loop region, which is missing in PXR.2. Yeast two-hybrid assays revealed that, even in the presence of ligand, the corepressors remain tightly bound to PXR.2, and coactivators are unable to bind at helix 12. In summary, PXR.2 can bind to PXREs but fails to transactivate target genes because ligands do not bind the ligand binding domain of PXR.2 productively, corepressors remain tightly bound, and coactivators are not recruited to PXR.2.

| S-EPMC2683691 | biostudies-literature

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