Perfluorooctanoic acid-induced toxicities in chicken embryo primary cardiomyocytes: Roles of PPAR alpha and Wnt5a/Frizzled2.
Animals
Calcium
/ metabolism
Caprylates
/ toxicity
Cardiotoxicity
Cells, Cultured
Chick Embryo
Environmental Pollutants
/ toxicity
Fluorocarbons
/ toxicity
Frizzled Receptors
/ metabolism
Myocytes, Cardiac
/ drug effects
PPAR alpha
/ metabolism
Signal Transduction
/ drug effects
Wnt-5a Protein
/ metabolism
Perfluorooctanoic acid
Wnt5a/Frizzled2
in ovo gene silencing
intracellular calcium
primary cardiomyocyte
Journal
Toxicology and applied pharmacology
ISSN: 1096-0333
Titre abrégé: Toxicol Appl Pharmacol
Pays: United States
ID NLM: 0416575
Informations de publication
Date de publication:
15 10 2019
15 10 2019
Historique:
received:
28
05
2019
revised:
25
07
2019
accepted:
18
08
2019
pubmed:
25
8
2019
medline:
19
5
2020
entrez:
25
8
2019
Statut:
ppublish
Résumé
Perfluorooctanoic acid (PFOA) is a widespread persistent organic pollutant and may induce developmental toxicities, including developmental cardiotoxicity. To explore the potential mechanism of developmental cardiotoxicity induced by PFOA exposure, chicken embryo primary cardiomyocytes were extracted either from chicken embryos pretreated with PFOA (2 mg/kg), or from untreated embryos and then directly exposed cells to PFOA (1, 10, 30 or 100 μg/ml) in culture. Additionally, peroxisome proliferator activated receptor alpha (PPAR alpha) silencing lentivirus was applied to the embryos on embryonic day (ED2). Cell viability was measured with CCK-8 kit, morphology was assessed with hematoxylin and eosin staining, and intracellular Ca
Identifiants
pubmed: 31445018
pii: S0041-008X(19)30324-2
doi: 10.1016/j.taap.2019.114716
pii:
doi:
Substances chimiques
Caprylates
0
Environmental Pollutants
0
Fluorocarbons
0
Frizzled Receptors
0
PPAR alpha
0
Wnt-5a Protein
0
perfluorooctanoic acid
947VD76D3L
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
114716Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.