Perfluorooctane sulfonic acid (PFOS) inhibits vessel formation in a human 3D co-culture angiogenesis model (NCFs/HUVECs).
3D co-culture
Angiogenesis
PFOS
Perfluorooctane sulfonic acid
VEGFR2
Vessel formation
Journal
Environmental pollution (Barking, Essex : 1987)
ISSN: 1873-6424
Titre abrégé: Environ Pollut
Pays: England
ID NLM: 8804476
Informations de publication
Date de publication:
15 Jan 2022
15 Jan 2022
Historique:
received:
03
06
2021
revised:
15
10
2021
accepted:
15
11
2021
pubmed:
21
11
2021
medline:
30
12
2021
entrez:
20
11
2021
Statut:
ppublish
Résumé
Perfluorooctane sulfonic acid (PFOS) is a ubiquitous environmental pollutant. In humans, PFOS exposure has been associated with a number of adverse health outcomes, including reduced birth weight. Whether PFOS is capable of affecting angiogenesis and thus possibly fetal development is unknown. Therefore, we investigated 1) the metabolic activity of PFOS-exposed endothelial cells (human umbilical vein endothelial cells, HUVECs), fibroblasts (normal colon fibroblasts, NCFs), and epithelial cells (human colorectal carcinoma cells, HCT116), 2) PFOS-specific inhibition of vascular endothelial growth factor receptor (VEGFR)2 stimulation in KDR/NFAT-RE HEK293 cells, and 3) the antiangiogenic potential of PFOS in a 3D in vitro angiogenesis model of HUVECs and NCFs. In terms of metabolic activity, endothelial cells (HUVECs) were much more sensitive to PFOS than fibroblasts (NCFs) or epithelial cells (HCT116). VEGFR2 signaling in KDR/NFAT-RE HEK293 cells decreased with increasing PFOS concentrations. In co-culture (angiogenesis assay), PFOS treatment resulted in a dose-dependent reduction in tip and branch formation, tip length (μm), and total structural area (μm
Identifiants
pubmed: 34800587
pii: S0269-7491(21)02125-4
doi: 10.1016/j.envpol.2021.118543
pii:
doi:
Substances chimiques
Alkanesulfonic Acids
0
Fluorocarbons
0
Vascular Endothelial Growth Factor A
0
perfluorooctane sulfonic acid
9H2MAI21CL
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
118543Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Ltd.. All rights reserved.