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Mus musculus

ABSTRACT: Gene expression profiling and TF occupancy upon treatment with the FXR agonist obeticholic acid

PROVIDER: PRJNA297442 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2541540.fastq.gz	Fastqsanger.gz
	SRR2541541.fastq.gz	Fastqsanger.gz
	SRR2541542.fastq.gz	Fastqsanger.gz
	SRR2541543.fastq.gz	Fastqsanger.gz
	SRR2541544.fastq.gz	Fastqsanger.gz

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Mus musculus

Project description:Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid [mouse]

| PRJNA306504 | ENA

Gene expression profiling and TF occupancy upon treatment with the FXR agonist obeticholic acid

Project description:The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids and regulates bile acid metabolism, glucose and cholesterol homeostasis. From mouse studies we know that the novel FXR agonist obeticholic acid (OCA) regulates expression of many genes in the liver, but there is currently no data on the effects of OCA on human liver gene expression. This is especially relevant since the novel FXR agonist OCA is currently tested in clinical trials for the treatment of several diseases, such as nonalcoholic steatohepatitis (NASH), nonalcoholic fatty liver disease (NAFLD) and Type 2 Diabetes. In this study we investigate the effect of OCA treatment on gene expression profiles and localization of FXR to the genome in relevant liver samples. ChIP-Seq for FXR in Liver tissue from 2 male mice treated with OCA/INT-747 (10mg/kg/day) and 2 male mice treated with vehicle (1% methyl cellulose).

2016-01-27 | E-GEOD-73624 | biostudies-arrayexpress

Mus musculus

Project description:Obeticholic acid induces hepatoxicity via FXR

| PRJNA701084 | ENA

Gene expression profiling and TF occupancy upon treatment with the FXR agonist obeticholic acid

2016-01-27 | GSE73624 | GEO

FXR isoform selective transcriptional activation in mouse liver organoids

Project description:The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids that regulates metabolic processes. FXR is expressed as four isoforms (α1-4), and their relative abundance is specific to tissue and bio-energetic conditions (Correia JC et al. 2015). Depending on the FXR isoform expressed, there is a degree of selectivity in target-genes activation. In this dataset, we defined FXR-isoforms selective effects on transcription in mouse liver organoids after treatment with the FXR agonist Obeticholic acid(OCA). By linking the DNA binding profiles of the FXR isoforms with their transcriptional output, we concluded that differential DNA binding plays a defining role in FXR-isoform target gene selectivity.

2020-07-27 | GSE133734 | GEO

FXR isoform selective effects on hepatoma cell line HepG2

Project description:The farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids that regulates bile acid metabolism, glucose and cholesterol homeostasis. FXR is expressed as four isoforms (α1-4), and their relative abundance is tissue specific. Human livers express predominantly FXR isoforms α1 and α2. From mouse studies we know that the FXR agonist obeticholic acid (OCA) regulates expression of many genes in the liver. However, there is currently no data on the effects of OCA on FXR isoform selective gene regulation. This is particularly relevant since the relative FXR isoform amounts in the liver are regulated by general bioenergetic cues (Correia JC et al. 2015). In this study we investigate the effect of variations in FXR isoforms α1 or α2 expression on HepG2 cell lines response to treatment with OCA.

2020-07-27 | GSE133659 | GEO

Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid

Project description:Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid

| PRJNA306501 | ENA

Homo sapiens

Project description:Gene expression profiling in human precision-cut liver slices upon treatment with the FXR agonist obeticholic acid [human]

| PRJNA306505 | ENA

FXR protects against neonatal sepsis via enhancing the immunosuppressive function of MDSCs

Project description:The presence of myeloid-derived suppressor cells (MDSCs) during the early postnatal period plays a protective role against neonatal inflammation. However, the mechanisms regulating neonatal MDSCs remain to be fully elucidated. In this study, we report that the bile acid receptor Farnesoid X receptor (FXR) acts as a pivotal positive regulator of neonatal MDSCs. Using FXR-deficient (FXR-/-) mice and FDA-approved FXR agonist obeticholic acid (OCA), we demonstrated that FXR deficiency impairs the immunosuppressive and antibacterial functions of neonatal MDSCs, thereby exacerbating the severity of neonatal sepsis. Adoptive transfer of MDSCs alleviates sepsis severity in FXR-/- neonatal pups. Mechanistic studies reveal that HIF1a, a well-established regulator of MDSCs, is a direct transcriptional target of FXR. Patients with neonatal sepsis displayed reduced MDSC frequencies and impaired expression of FXR and HIF-1α, which was negatively correlate with the clinical parameters. These observations highlight the important role of FXR in neonatal MDSCs and its therapeutic potential in neonatal sepsis.

2025-05-20 | GSE289598 | GEO

Tropifexor-Mediated Abrogation of Steatohepatitis and Fibrosis Is Associated With Antioxidative Gene Expression Profile in Rodents

Project description:Farnesoid X receptor (FXR) agonism is emerging as an important potential therapeutic mechanism of action for multiple chronic liver diseases. The bile acid–derived FXR agonist obeticholic acid (OCA; 6-ethyl chenodeoxycholic acid) has shown promise in a phase 2 study in patients with nonalcoholic steatohepatitis (NASH). Here, we report efficacy of a novel, non–bile acid FXR agonist tropifexor (LJN452) in two distinct preclinical models of NASH. The efficacy of tropifexor at <1 mg/kg doses was superior to that of OCA at 25 mg/kg in the liver in both NASH models. In a chemical and dietary model of NASH (STAM model), tropifexor reversed established fibrosis and reduced nonalcoholic fatty liver disease activity score and hepatic triglycerides. In an insulin-resistant, obese NASH model (AMLN), tropifexor markedly reduced steatohepatitis, fibrosis, and profibrogenic gene expression. Transcriptome analysis of livers from AMLN mice revealed 461 differentially expressed genes following tropifexor treatment, which included a combination of signatures associated with reduction of oxidative stress, fibrogenesis, and inflammation. Conclusion: Based on the preclinical validation in animal models, tropifexor is a promising investigational therapy that is currently under phase 2 development for NASH.

2019-08-20 | GSE129389 | GEO

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