Different effects of GsMTx4 on nocturia associated with the circadian clock and Piezo1 expression in mice.
Animals
CLOCK Proteins
/ genetics
Disease Models, Animal
Gene Expression
/ drug effects
Injections, Intraperitoneal
Intercellular Signaling Peptides and Proteins
/ administration & dosage
Ion Channels
/ antagonists & inhibitors
Male
Mice
Mice, Inbred C57BL
Mutation
/ drug effects
Nocturia
/ drug therapy
Spider Venoms
/ administration & dosage
GsMTx4
Nocturia
Piezo1
Journal
Life sciences
ISSN: 1879-0631
Titre abrégé: Life Sci
Pays: Netherlands
ID NLM: 0375521
Informations de publication
Date de publication:
01 Aug 2021
01 Aug 2021
Historique:
received:
08
02
2021
revised:
06
04
2021
accepted:
19
04
2021
pubmed:
1
5
2021
medline:
25
6
2021
entrez:
30
4
2021
Statut:
ppublish
Résumé
Nocturia is a major problem in geriatric patients. Clock genes regulate circadian bladder function and Piezo type mechanosensitive ion channel component 1 (Piezo1) that senses bladder fullness. We utilized WT and Clock mutant (Clock We compared voiding behavior in mice after the administration of vehicle, low dose, or high dose of GsMTx4. Intraperitoneal injections (IP) were performed at Zeitgeber time (ZT) 0, lower Piezo1 expression phase (ZT0-IP) and ZT12, higher Piezo1 expression phase (ZT12-IP). Urine volume (Uvol), voiding frequency (VF), and urine volume per void (Uvol/v) were measured using metabolic cages. VF decreased at ZT12-IP in WT mice only with high dose of GsMTx4 but showed no effects in Clock The effects of GsMTx4 changed associated with the circadian clock and Piezo1 expression level. The maximum effect occurred during sleep phase in WT. These results may lead to new therapeutic strategies against nocturia.
Identifiants
pubmed: 33930366
pii: S0024-3205(21)00541-5
doi: 10.1016/j.lfs.2021.119555
pii:
doi:
Substances chimiques
Intercellular Signaling Peptides and Proteins
0
Ion Channels
0
MTx4 protein, Grammostola spatulata
0
Piezo1 protein, mouse
0
Spider Venoms
0
CLOCK Proteins
EC 2.3.1.48
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
119555Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.