Endocannabinoids and endocannabinoid-like compounds modulate hypoxia-induced permeability in CaCo-2 cells via CB
2-Arachidonoylglycerol (2-AG)
Anandamide (AEA)
Caco-2 cells
Cannabinoid receptor 1 (CB(1))
Cannabinoid receptors
Endocannabinoids
Hypoxia
Intestinal permeability
Ischaemia
N-arachidonoyl-dopamine (NADA)
Noladin ether (NE)
Oleamide (OA)
Peroxisome proliferator-activated receptor alpha (PPARα)
Transepithelial electrical resistance (TEER)
Transient receptor potential vanilloid subtype 1 (TRPV1)
Virodhamine (VD)
Journal
Biochemical pharmacology
ISSN: 1873-2968
Titre abrégé: Biochem Pharmacol
Pays: England
ID NLM: 0101032
Informations de publication
Date de publication:
10 2019
10 2019
Historique:
received:
13
03
2019
accepted:
15
07
2019
pubmed:
22
7
2019
medline:
2
7
2020
entrez:
21
7
2019
Statut:
ppublish
Résumé
We have previously reported that endocannabinoids modulate permeability in Caco-2 cells under inflammatory conditions and hypothesised in the present study that endocannabinoids could also modulate permeability in ischemia/reperfusion. Caco-2 cells were grown on cell culture inserts to confluence. Trans-epithelial electrical resistance (TEER) was used to measure permeability. To generate hypoxia (0% O Complete hypoxia decreased TEER (increased permeability) by ~35% after 4 h (recoverable) and ~50% after 6 h (non-recoverable). When applied either pre- or post-hypoxia, apical application of N-arachidonoyl-dopamine (NADA, via TRPV1), oleamide (OA, via TRPV1) and oleoylethanolamine (OEA, via TRPV1) inhibited the increase in permeability. Apical administration of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) worsened the permeability effect of hypoxia (both via CB A variety of endocannabinoids and endocannabinoid-like compounds modulate Caco-2 permeability in hypoxia/reoxygenation, which involves multiple targets, depending on whether the compounds are applied to the basolateral or apical membrane. CB
Sections du résumé
BACKGROUND AND PURPOSE
We have previously reported that endocannabinoids modulate permeability in Caco-2 cells under inflammatory conditions and hypothesised in the present study that endocannabinoids could also modulate permeability in ischemia/reperfusion.
EXPERIMENTAL APPROACH
Caco-2 cells were grown on cell culture inserts to confluence. Trans-epithelial electrical resistance (TEER) was used to measure permeability. To generate hypoxia (0% O
KEY RESULTS
Complete hypoxia decreased TEER (increased permeability) by ~35% after 4 h (recoverable) and ~50% after 6 h (non-recoverable). When applied either pre- or post-hypoxia, apical application of N-arachidonoyl-dopamine (NADA, via TRPV1), oleamide (OA, via TRPV1) and oleoylethanolamine (OEA, via TRPV1) inhibited the increase in permeability. Apical administration of anandamide (AEA) and 2-arachidonoylglycerol (2-AG) worsened the permeability effect of hypoxia (both via CB
CONCLUSIONS AND IMPLICATIONS
A variety of endocannabinoids and endocannabinoid-like compounds modulate Caco-2 permeability in hypoxia/reoxygenation, which involves multiple targets, depending on whether the compounds are applied to the basolateral or apical membrane. CB
Identifiants
pubmed: 31325449
pii: S0006-2952(19)30272-2
doi: 10.1016/j.bcp.2019.07.017
pii:
doi:
Substances chimiques
Endocannabinoids
0
PPAR alpha
0
Receptor, Cannabinoid, CB1
0
TRPV Cation Channels
0
TRPV1 protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
465-472Informations de copyright
Copyright © 2019. Published by Elsevier Inc.