Crosstalk between the aryl hydrocarbon receptor and hypoxia-inducible factor 1α pathways in human islet models.

ABSTRACT:

Background

We previously showed that 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD - a persistent organic pollutant) activates the aryl hydrocarbon receptor (AHR) in pancreatic islets. The AHR is known to crosstalk with hypoxia-inducible factor 1α (HIF1α) in other cell types but AHR-HIF1α crosstalk has not been previously examined in islet cells. Islet cell function is sensitive to hypoxia; we hypothesize that AHR activation by environmental pollutant(s) will interfere with the HIF1α pathway response in islets, which may be detrimental to islet cell function and survival during periods of hypoxia.

Methods

We assessed AHR-HIF1α crosstalk by treating human donor islets and stem cell-derived islets (SC-islets) with 10 nM TCDD ± 1% O₂ and measuring gene expression of down

SUBMITTER: Gang N 

PROVIDER: S-EPMC12279269 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature