TRPV4-Mediated Regulation of the Blood Brain Barrier Is Abolished During Inflammation.
TRPV4
blood brain barrier
experimental autoimmune encephalomyelitis
stroke
transendothelial resistance
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2020
2020
Historique:
received:
29
04
2020
accepted:
07
08
2020
entrez:
25
9
2020
pubmed:
26
9
2020
medline:
26
9
2020
Statut:
epublish
Résumé
Blood-brain barrier (BBB) dysfunction is critically involved in determining the extent of several central nervous systems (CNS) pathologies and here in particular neuroinflammatory conditions. Inhibiting BBB breakdown could reduce the level of vasogenic edema and the number of immune cells invading the CNS, thereby counteracting neuronal injury. Transient receptor potential (TRP) channels have an important role as environmental sensors and constitute attractive therapeutic targets that are involved in calcium homeostasis during pathologies of the CNS. Transient receptor potential vanilloid 4 (TRPV4) is a calcium permeable, non-selective cation channel highly expressed in endothelial cells. As it is involved in the regulation of the blood brain barrier permeability and consequently cerebral edema formation, we anticipated a regulatory role of TRPV4 in CNS inflammation and subsequent neuronal damage. Here, we detected an increase in transendothelial resistance in mouse brain microvascular endothelial cells (MbMECs) after treatment with a selective TRPV4 inhibitor. However, this effect was abolished after the addition of IFNγ and TNFα indicating that inflammatory conditions override TRPV4-mediated permeability. Accordingly, we did not observe a protection of
Identifiants
pubmed: 32974355
doi: 10.3389/fcell.2020.00849
pmc: PMC7481434
doi:
Types de publication
Journal Article
Langues
eng
Pagination
849Informations de copyright
Copyright © 2020 Rosenkranz, Shaposhnykov, Schnapauff, Epping, Vieira, Heidermann, Schattling, Tsvilovskyy, Liedtke, Meuth, Freichel, Gelderblom and Friese.
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