TRPV4 Mediates Acute Bladder Responses to Bacterial Lipopolysaccharides.
Animals
Antigens, Bacterial
/ immunology
Calcium
/ metabolism
Cells, Cultured
Cystitis
/ immunology
Humans
Lipopolysaccharides
/ immunology
Mice
Mice, Inbred C57BL
Mice, Knockout
NF-kappa B
/ metabolism
Protein Transport
TRPV Cation Channels
/ genetics
Urinary Bladder
/ immunology
Urothelium
/ metabolism
LPS
TRPV4
bladder
cystitis
urothelial cells
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2020
2020
Historique:
received:
31
01
2020
accepted:
07
04
2020
entrez:
22
5
2020
pubmed:
22
5
2020
medline:
18
3
2021
Statut:
epublish
Résumé
Urinary tract infections (UTI) affect a large proportion of the population, causing among other symptoms, more frequent and urgent micturition. Previous studies reported that the gram-negative bacterial wall component lipopolysaccharides (LPS) trigger acute epithelial and bladder voiding responses, but the underlying mechanisms remain unknown. The cation channel TRPV4 is implicated in the regulation of the bladder voiding. Since TRPV4 is activated by LPS in airway epithelial cells, we sought to determine whether this channel plays a role in LPS-induced responses in urothelial cells (UCs). We found that human-derived UCs display a fast increase in intracellular Ca
Identifiants
pubmed: 32435246
doi: 10.3389/fimmu.2020.00799
pmc: PMC7218059
doi:
Substances chimiques
Antigens, Bacterial
0
Lipopolysaccharides
0
NF-kappa B
0
TRPV Cation Channels
0
Trpv4 protein, mouse
0
Calcium
SY7Q814VUP
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
799Informations de copyright
Copyright © 2020 Alpizar, Uvin, Naert, Franken, Pinto, Sanchez, Gevaert, Everaerts, Voets, De Ridder and Talavera.
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