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PXR-gut microbiota interaction

ABSTRACT: Pregnane X receptor is a sexually dimorphic hepatic effector of gut microbiota involved in the host's lipid and xenobiotic metabolism

PROVIDER: PRJEB39629 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR4386470_1.fastq.gz	Fastqsanger.gz
	ERR4386470_2.fastq.gz	Fastqsanger.gz
	ERR4386480_1.fastq.gz	Fastqsanger.gz
	ERR4386480_2.fastq.gz	Fastqsanger.gz
	ERR4386490_1.fastq.gz	Fastqsanger.gz

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The pregnane X receptor drives sexually dimorphic hepatic changes in lipid and xenobiotic metabolism in response to gut microbiota in mice

Project description:The gut microbiota-intestine-liver relationship is emerging as an important factor in multiple hepatic pathologies, but the hepatic sensors and effectors of microbial signals are not well defined. By comparing publicly available liver transcriptomics data from conventional vs. germ-free mice, we identified pregnane X receptor (PXR, NR1I2) transcriptional activity as strongly affected by the absence of gut microbes. Microbiota depletion in Pxr+/+ vs Pxr-/- C57Bl6/J mice revealed that most microbiota-sensitive genes were PXR-dependent in the liver in males, but not in females. Pathway enrichment analysis revealed that microbiota-PXR interaction controlled fatty-acid and xenobiotic metabolism. Antibiotic treatment reduced liver triglyceride content and hampered xenobiotic metabolism in livers from Pxr+/+ but not Pxr-/- male mice. These findings identify PXR as a hepatic effector of sexually dimorphic responses to microbiota-derived signals and reveal a potential new mechanism for unexpected drug-drug or food-drug interactions.

2020-08-26 | GSE156837 | GEO

The pregnane X receptor drives sexually dimorphic hepatic changes in lipid and xenobiotic metabolism in response to gut microbiota in mice

Project description:The pregnane X receptor drives sexually dimorphic hepatic changes in lipid and xenobiotic metabolism in response to gut microbiota in mice

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Hepatic BCL6 and plasma triglycerides regulate sexual dimorphism in tissue tolerance [set 5]

Project description:Tissue tolerance is a sexually dimorphic trait. Here, we investigated the role of BCL6 in establishing hepatic chromatin landscape promoting sexually dimorphic tissue tolerance during E.Coli infection.

2022-10-21 | GSE138395 | GEO

Effect of somatostatin knockout on sexually dimorphic hepatic gene expression

Project description:The liver is one of the most sexually dimorphic organs as measured by gene expression differences. About 80% of the sexually dimorphic genes are known to be regulated by growth hormone (GH). Somatostatin (SST) inhibits the release of GH. We generated a SST-knockout mouse and analyzed the hepatic gene expression changes in both sexes.

2014-12-01 | GSE56520 | GEO

Hepatic BCL6 and plasma triglycerides regulate sexual dimorphism in tissue tolerance [set 4]

Project description:Hepatic gene expression shows sexual dimorphism. Here, we investigated the role of BCL6 in establishing sexually dimorphic chromatin state and performed H3K27ac ChIP-seq from livers of female and male Ctrl and BCL6 liver knock-out mice.

2022-10-21 | GSE138393 | GEO

Transcriptional profiling of liver from wild type and PXR-null mice treated with PCN

Project description:Many environmentally-relevant chemicals and drugs activate the nuclear receptor pregnane X receptor (PXR). Activation of PXR can lead to increases in liver weight in part through hepatocyte replication similar to a large number of compounds that activate other nuclear receptors such as the peroxisome proliferator-activated receptor alpha and the constitutive activated receptor (CAR). PXR controls the expression of a large battery of genes involved in xenobiotic metabolism. Identification of genes that are accurate predictors of PXR activation would be useful in high-throughput screens to assess potential toxicity and drug-drug interactions. Here, we identified PXR-dependent genes in the mouse liver after exposure to pregnenolone 16alpha-carbinonitrile (PCN), a chemical that is often used as a model PXR agonist.

2014-09-30 | GSE55746 | GEO

Mus musculus

Project description:Effect of somatostatin knockout on sexually dimorphic hepatic gene expression

| PRJNA243621 | ENA

Corticosteroid-binding globulin (SERPINA6) consolidates sexual dimorphism of adult rat liver

Project description:Produced by the liver, corticosteroid-binding globulin (CBG) regulates the plasma distribution and actions of glucocorticoids. A sex difference in pituitary growth hormone secretion patterns established during puberty in rats results in increased hepatic CBG production and two-fold higher plasma corticosterone levels in females. Glucocorticoids control hepatic development and metabolic activities, and we have therefore examined how disrupting the SerpinA6 gene encoding CBG influences plasma corticosterone dynamics, as well as liver gene expression in male and female rats before and after puberty. Comparisons of corticosterone plasma clearance and hepatic uptake in adult rats, with or without CBG, indicated that CBG limits corticosterone clearance by reducing its hepatic uptake. Hepatic transcriptomic profiling revealed minor sex differences (207 differentially expressed genes) and minimal effect of CBG deficiency in 30-day-old rats before puberty. While liver transcriptomes in 60-day-old males lacking CBG remained essentially unchanged, 2,710 genes were differentially expressed in wild-type female versus male livers at this age. Importantly, ~10% of these genes lost their sexually dimorphic expression in adult females lacking CBG, including those related to cholesterol biosynthesis, inflammation, and lipid and amino acid catabolism. Another 203 genes were altered by the loss of CBG specifically in adult females, including those related to xenobiotic metabolism, circadian rhythm, and gluconeogenesis. Our findings reveal that CBG consolidates the sexual dimorphism of the rat liver initiated by sex differences in growth hormone secretion patterns and provide insight into how CBG deficiencies are linked to glucocorticoid-dependent diseases.

2023-11-03 | GSE245348 | GEO

B3galt5 regulates obesity and insulin resistance by maintaining the intestinal integrity as a novel PXR target gene

Project description:Pregnane X receptor (PXR), a xenobiotic receptor involved in drug metabolism, has been reported to regulate lipid and glucose metabolism. The intestine tract is the first inner barrier of the body, which dysfunction contributes to the development of metabolic disorders. However, the role of intestinal PXR in metabolic diseases remains largely unknown. In this study, we showed that activation of PXR by tributyl citrate (TBC), an intestinal-selective agonist of PXR, improved high fat diet (HFD)-induced obesity and insulin resistance. The metabolic benefit of intestinal PXR activation was associated with upregulation of β-1,3 galactosyltransferase 5 (B3galt5). Our results revealed that B3galt5 is mainly expressed in the intestine and is a direct transcriptional target of PXR. Whole-body and intestine-specific knockout of B3galt5 exacerbated HFD-induced obesity, insulin resistance and inflammation. Mechanistically, B3galt5 is essential to maintain the integrity of intestinal mucus barrier. Ablation of B3galt5 impaired the O-glycosylation of mucin2, destabilized the mucus layer, and increased the permeability of intestinal barrier. Furthermore, B3galt5 deficiency abolished the beneficial effect of intestinal PXR activation on metabolic disorders. Our results suggested the intestinal-selective activation of PXR regulated B3galt5 expression holds an important role in maintaining metabolic homeostasis, making it a potential therapeutic strategy in obesity.

2024-07-02 | GSE266942 | GEO

Pregnane X Receptor (PXR) protects against cisplatin-induced acute kidney injury

Project description:Background: Cisplatin-induced acute kidney injury (CAKI) has been recognized as one of the most serious side effects of cisplatin. Pregnane X receptor (PXR) is a ligand-dependent nuclear receptor and serves as a master regulator of xenobiotic detoxification. Increasing evidence also suggests PXR has many nonxenobiotic functions including the regulation of cell proliferation, inflammatory response and glucose and lipid metabolism. Methods: In this study, we aimed to investigate the role of PXR in cisplatin-induced nephrotoxicity. CAKI model was performed in wild-type or PXR knockout mice. Pregnenolone 16α-carbonitrile (PCN), a mouse PXR specific agonist, was used for PXR activation. The renal function, biochemical, histopathological and molecular alterations were examined in mouse blood, urine or renal tissues. Whole transcriptome analysis was performed by RNA sequencing. Dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays were applied to determine the regulation of PXR on its target genes. Results: We found that PXR activation significantly attenuated CAKI as reflected by improved renal function, reduced renal tubular apoptosis, ameliorated oxidative and endoplasmic reticulum stress, and suppressed inflammatory factor expression. RNA sequencing analysis revealed that the renoprotective effect of PXR was associated with multiple crucial signaling pathways. In particular, PXR protected against cisplatin-induced AKI by the activation of PI3K/AKT pathway and the induction of multidrug and toxin extrusion 1 (MATE1), an important transporter mediating cellular excretion of cisplatin, in the kidney. Conclusions: Our results demonstrate that PXR activation can preserve renal function in cisplatin-induced AKI and suggest a possibility of PXR as a novel therapeutic target for cisplatin-induced nephrotoxicity.

2023-03-20 | GSE147256 | GEO

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