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

ABSTRACT: 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.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Endothelial Cell Of Umbilical Vein, Cell Culture

DISEASE(S): Disease Free

SUBMITTER: Si-yan Zhang  

LAB HEAD: Jing Zheng

PROVIDER: PXD047834 | Pride | 2025-02-10

REPOSITORIES: Pride