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Activation of AHR transcriptional activity upon treatment with indole-3-pyruvate

ABSTRACT: Activation of AHR transcriptional activity upon treatment with indole-3-pyruvate

PROVIDER: PRJNA599381 | ENA |

REPOSITORIES: ENA

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Activation of AHR transcriptional activity upon treatment with indole-3-pyruvate

Project description:Indole-3-pyruvate (I3P), an endogenous metabolite derived from tryptophan by gut microbiota and IL4I1 enzyme in humans can potentially activate the transcriptional activity of the Aryl Hydrocarbon receptor. Here we test this by stimulating AHR proficient U-87MG cells with I3P alone or in combination with the AHR antagonist SR1.

2020-08-19 | GSE143240 | GEO

Analysis of HeLa cell transcriptome changes induced by Indole-3-pyruvate and mIL4i1

Project description:We analyzed the mRNA changes induced by Indole-3-pyruvate (I3P) and WT or K351A mutant mIL4i1 in HeLa cells.

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Analysis of THP-1 cell transcriptome changes induced by Phenylpyruvate, 4-Hydroxyphenylpyruvate and Indole-3-pyruvate

Project description:We analyzed the mRNA changes iduced by the alpha keto acids Phenylpyruvate (PP), 4-Hydroxyphenylpyruvate (4HPP) or Indole-3-pyruvate (I3P) in THP-1 cells.

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Gut Microbiota Metabolite Indole-3-Acetic Acid Maintains Intestinal Epithelial Homeostasis via the transcription factor AHR

Project description:The incidence and prevalence of inflammatory bowel disease (IBD) is gradually increasing. A high-fat diet (HFD) is known to disrupt intestinal homeostasis and aggravate IBD, yet the underlying mechanisms remain largely undefined. Here, a positive correlation between dietary fat intake and disease severity in both IBD patients and HFD-fed mice is observed. HFD induces a significant decrease in indole-3-acetic acid (IAA) and lead to intestinal barrier damage. Furthermore, IAA supplementation enhances the intestinal mucin sulfation and effectively alleviates colitis. Mechanistically, IAA upregulates key molecules involved in mucin sulfation, including Papss2 and Slc35b3, the synthesis enzyme and the transferase of 3'-phosphoadenosine-5'-phosphosulfate (PAPS), via the Aryl Hydrocarbon Receptor (AHR). More importantly, AHR can directly bind to the transcription start site of Papss2. Oral administration of Lactobacillus reuteri, which can produce IAA, contributes to protecting against colitis and promoting mucin sulfation, while the modified L. reuteri strain lacking the iaaM gene (LactobacillusΔiaaM) and the ability to produce IAA fails to exhibit such effects. Overall, IAA enhances intestinal mucin sulfation through AHR, contributing to the protection of intestinal homeostasis.

2025-12-11 | GSE255130 | GEO

Proteomic characterization of the cellular effects of AHR activation by microbial tryptophan catabolites in endotoxin-activated human macrophages

Project description:Sensing of microbial tryptophan catabolites by the aryl hydrocarbon receptor (AhR) plays a pivotal role in host-microbiome homeostasis by modulating the host immune response. Thereby the involved cellular processes triggered by the metabolites are largely unknown. We analyzed proteomic changes in macrophages trough 24h after treatment with the tryptophan metabolites indole-3-acetic acid (I3AA) or indole-3-aldehyde (IAld), as well as the prototypic AhR-ligand Benzo(a)pyrene (BaP) in the absence and presence of LPS to identify affected processes and pathways.

2021-11-03 | PXD025022 | Pride

Analysis of HeLa cell transcriptome changes induced by Indole-3-pyruvate and mIL4i1

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Hexokinase 2 is a transcriptional targetHexokinase 2 is a transcriptional target and a positive modulator of AHR signalling and a positive modulator of AHR signalling

Project description:The Aryl Hydrocarbon Receptor (AHR) regulates the expression of numerous genes in response to activation by agonists including xenobiotics. Although it is well appreciated that environmental signals and cell intrinsic features may modulate this transcriptional response, how it is mechanistically achieved remains poorly understood. We show that Hexokinase 2 (HK2) a metabolic enzyme fuelling cancer cell growth, is a transcriptional target of AHR as well as a modulator of its activity. Expression of HK2 is positively regulated by AHR upon exposure to agonists both in human cells and in mice lung tissues. Conversely, over-expression of HK2 regulates the abundance of many proteins involved in the regulation of AHR signalling and these changes are linked with altered AHR expression levels and transcriptional activity. HK2 expression also shows a negative correlation with AHR promoter methylation in tumours, and these tumours with high HK2 expression and low AHR methylation are associated with a worse overall survival in patients. In sum, our study provides novel insights into how AHR signalling is regulated which may help our understanding of the context-specific effects of this pathway and may have implications in cancer.

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AhR activity directs BRAF inhibitors resistance in metastastic melanoma

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Project description:Macrophages that acquire an immunosuppressive phenotype are crucial for creating the pre-metastatic niche (PMN), which is essential for facilitating breast cancer metastasis to the distant organ. Our study showed that increased aryl hydrocarbon receptor (AHR) activity in lung macrophages is vital for establishing the immunosuppressive PMN in breast cancer. AHR activation led to higher PD-L1 expression on macrophages through directly binding to the promoter of Pdl1, subsequently, promoting Treg cell differentiation in the PMN. Mice with Ahr conditional deletion in macrophages had reduced lung metastasis of breast cancer. The elevated AHR level in PMN macrophages was induced by GM-CSF released from breast cancer cells, which activated STAT5 and prevented AHR ubiquitination in macrophages. In breast cancer patients, the expression of AHR and PD-L1 correlated with Treg cell infiltration, and high AHR expression was associated with a poor prognosis. Our findings uncover a previously unknown cellular and molecular mechanism through which macrophages establish the lung PMN in breast cancer.

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