Inhibition of GPR91 Reduces Inflammatory Mediators Involved in Active Labor in Myometrium.
Journal
Mediators of inflammation
ISSN: 1466-1861
Titre abrégé: Mediators Inflamm
Pays: United States
ID NLM: 9209001
Informations de publication
Date de publication:
2020
2020
Historique:
received:
01
12
2019
revised:
25
02
2020
accepted:
12
03
2020
entrez:
8
5
2020
pubmed:
8
5
2020
medline:
18
5
2021
Statut:
epublish
Résumé
GPR91 mRNA expression was significantly higher in myometrium from women during term spontaneous labor compared to no labor. Likewise, in mice, GPR91 mRNA expression was significantly upregulated in myometrium during inflammation-induced preterm labor compared to preterm no labor. In myometrial cells, IL1B and TNF significantly increased GPR91 mRNA expression. Knockdown of GPR91 by siRNA in myometrial cells significantly suppressed the secretion and/or expression of IL1B- and TNF-induced proinflammatory cytokines (GM-CSF, IL1A, IL1B, and IL6) and chemokines (CXCL8 and CCL2), myometrial contractility (expression of the contraction-associated proteins PTGFR and CX43, secretion of the uterotonic PGF Our findings demonstrate that GPR91 is involved in the genesis of proinflammatory and prolabor mediators induced by IL1B or TNF and collectively suggest that GPR91 may contribute to augmentation of the labor processes.
Identifiants
pubmed: 32377163
doi: 10.1155/2020/6454282
pmc: PMC7180404
doi:
Substances chimiques
Inflammation Mediators
0
NF-kappa B
0
Receptors, G-Protein-Coupled
0
SUCNR1 protein, human
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
6454282Informations de copyright
Copyright © 2020 Ratana Lim and Martha Lappas.
Déclaration de conflit d'intérêts
The authors have nothing to declare.
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