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Effect of canonical aryl hydrocarbon receptor pathway inhibitor on human endothelial cells

ABSTRACT: To study the effect of blockade of canonical aryl hydrocarbon receptor (AHR) pathway in human endothelial cells, we treated human umbilical vein endothelial cells (HUVECs) and adipose endothelial cells with a canonical AHR inhibitor, Stemreginin 1 (SR1) and performed bulk RNAseq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE298239 | GEO | 2025/07/23

REPOSITORIES: GEO

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Effect of canonical aryl hydrocarbon receptor pathway inhibitor on human umbilical vein endothelial cells

Project description:To study the effect of blockade of canonical aryl hydrocarbon receptor (AHR) pathway in human endothelial cells, we treated human umbilical vein endothelial cells (HUVECs) with a canonical AHR inhibitor, Stemreginin 1 (SR1) and performed bulk RNAseq analysis.

2024-07-01 | GSE251861 | GEO

Endogenous aryl hydrocarbon receptor ligands-dysregulated phosphoproteomes and proteomes in human fetal endothelial cells

Project description:Preeclampsia (PE) is a leading cause of maternal and fetal morbidity and mortality and is characterized by a wide spectrum of impaired maternal and fetal vascular function. Aryl hydrocarbon receptor (AhR, a ligand-activated transcription factor) plays a critical role in regulating vascular development and function. Endogenous AhR ligands can induce endothelial dysfunction. However, the underlying protein phospho-signaling mechanisms remain unknown. To determine if endogenous AhR ligands dysregulate the phosphoproteomes and proteomes in endothelial cells, primary human umbilical vein endothelial cells (HUVECs) (n = 4; 2 cell preparations/cell sex) were cultured in endothelial cell media (ECM). After 16 hr serum starvation, subconfluent cells were treated with 1 µM 2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE, an endogenous AhR ligand) or DMSO (vehicle) for 4 and 24 hr. The cell proteins were subjected to a bottom-up phosphoproteomic analysis to determine acute and prolonged effects of ITE on protein phosphorylation.

2025-02-10 | PXD047834 | Pride

Aryl hydrocarbon receptor antagonists promote the expansion of human hematopoietic stem cells

Project description:Although practiced clinically for more than 40 years, the use of hematopoietic stem cell (HSC) transplants remains limited by the ability to expand these cells ex vivo. An unbiased screen with primary human HSCs identified a purine derivative, StemRegenin 1 (SR1), that promotes the ex vivo expansion of CD34+ cells. Culture of HSCs with SR1 led to a 50-fold increase in cells expressing CD34 and a 17-fold increase in cells that retain the ability to engraft immunodeficient mice. Mechanistic studies show that SR1 acts by antagonizing the aryl hydrocarbon receptor (AHR). The identification of SR1 and AHR modulation as a means to induce ex vivo HSC expansion should facilitate the clinical use of HSC therapy. LGC006, a less potent SR1 analog, was also examined. KEYWORDS: two compounds, multiple doses, one time point two compounds, multiple doses, one time point

2011-04-04 | E-GEOD-28359 | biostudies-arrayexpress

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2011-04-04 | GSE28359 | GEO

Endogenous aryl hydrocarbon receptor ligands-dysregulated transcriptomic profiles and endothelial function in human fetal endothelial cells

Project description:Preeclampsia (PE) is a hypertensive disorder and a leading cause of maternal and fetal mortality and morbidity during human pregnancy. Aryl hydrocarbon receptor (AhR), a ligand-activated transcription factor, regulates vascular development and function during pregnancy. Here, we report the important role of endogenous AhR ligands in endothelial growth and function during pregnancy using human umbilical vein endothelial cells (HUVECs) as a model. We found that ITE, ([2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester], an endogenous AhR ligand) decreased cell proliferation and monolayer integrity in HUVECs in vitro. ITE also dysregulated transcriptomic profiles of HUVECs in a fetal sex-specific manner. The ITE-dysregulated genes were enriched in biological function and pathways highly relevant to cardiovascular diseases, vascular function, and inflammation responses. We conclude that dysregulation of endogenous AhR ligands may contribute to the PE-impaired endothelial function through fetal sex-specific regulation of endothelial transcriptomes. These AhR ligand-activated genes and pathways might represent promising therapeutic and sex-specific targets for PE-impaired endothelial function.

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Effect of canonical aryl hydrocarbon receptor pathway inhibitor on human endothelial cells

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Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

Project description:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.

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Project description:Acinetobacter baumannii is a highly pathogenic and multidrug-resistant Gram-negative bacterium that causes severe nosocomial infections. To better understand the mechanism of pathogenesis, we compare the proteomes of uninfected and infected human cells, revealing that transcription factor FOS is the host protein most strongly induced by A. baumannii infection. Pharmacological inhibition of FOS reduces the cytotoxicity of A. baumannii in cell-based models, and similar results are also observed in a mouse infection model. A. baumannii outer membrane vesicles (OMVs) are shown to activate the aryl hydrocarbon receptor (AHR) of host cells by inducing the host enzyme tryptophan-2,3-dioxygenase (TDO), producing the ligand kynurenine, which binds AHR. Following ligand binding, AHR is a direct transcriptional activator of the FOS gene. Our results suggest that bacterial infection interacts with host tryptophan metabolism and the transcription factor FOS.

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Expression data of primary melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice

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