Lack of NHE6 and Inhibition of NKCC1 Associated With Increased Permeability in Blood Labyrinth Barrier-Derived Endothelial Cell Layer.
NHE6/SLC9A6
NKCC1
blood-labyrinth barrier
cochlea
hearing loss
Journal
Frontiers in cellular neuroscience
ISSN: 1662-5102
Titre abrégé: Front Cell Neurosci
Pays: Switzerland
ID NLM: 101477935
Informations de publication
Date de publication:
2022
2022
Historique:
received:
25
01
2022
accepted:
17
03
2022
entrez:
2
5
2022
pubmed:
3
5
2022
medline:
3
5
2022
Statut:
epublish
Résumé
Acoustic trauma, autoimmune inner ear disease, and presbycusis feature loss of the integrity of the blood-labyrinth barrier (BLB). Normal BLB function depends on endothelial structural integrity, which is supported and maintained by tight junctions and adherens junctions within the microvascular endothelial layer. When these junctions are disrupted, vascular leakage occurs. Tight junctions and adherens junctions are functionally and structurally linked, but the exact signaling pathways underlying their interaction remain unknown. In addition, solute carriers (SC) are essential for optimal exchange through BLB. Previously, we found that SC family member, the sodium-hydrogen exchanger NHE6, was expressed in all wildtype cochlear tissues, and that
Identifiants
pubmed: 35496913
doi: 10.3389/fncel.2022.862119
pmc: PMC9039518
doi:
Types de publication
Journal Article
Langues
eng
Pagination
862119Informations de copyright
Copyright © 2022 Sekulic-Jablanovic, Paproth, Sgambato, Albano, Fuster, Bodmer and Petkovic.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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