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Endogenous aryl hydrocarbon receptor ligands-dysregulated transcriptomic profiles and vascular function in rat placentas

ABSTRACT: Endogenous aryl hydrocarbon receptor ligands-dysregulated transcriptomic profiles and vascular function in rat placentas

PROVIDER: PRJNA1053275 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27218900_1.fastq.gz	Fastqsanger.gz
	SRR27218900_2.fastq.gz	Fastqsanger.gz
	SRR27218901_1.fastq.gz	Fastqsanger.gz
	SRR27218901_2.fastq.gz	Fastqsanger.gz
	SRR27218902_1.fastq.gz	Fastqsanger.gz

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Endogenous aryl hydrocarbon receptor ligands-dysregulated transcriptomic profiles and vascular function in rat placentas

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 vascular growth and function during pregnancy using a rat model. We found that exposure of pregnant rats to an endogenous AhR ligand (ITE, [2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester]) elevated maternal blood pressure and induced proteinuria, while decreased uteroplacental blood flow and fetal/ placental growth, all of which are hallmarks of PE. ITE also dysregulated transcriptomic profiles of rat placentas in a fetal sex-specific manner. The ITE-dysregulated genes were enriched in biological function and pathways highly relevant to diseases of heart, liver, and kidney, vascular function, and inflammation responses. Collectively, we conclude that dysregulation of endogenous AhR ligands may contribute to the PE-impaired vascular function through fetal sex-specific regulation of immune cell infiltration and transcriptomes. These AhR ligand-activated genes and pathways might represent promising therapeutic and sex-specific targets for PE-impaired vascular function.

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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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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.

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