Inhibition of mPGES-1 attenuates efficient resolution of acute inflammation by enhancing CX3CL1 expression.
Animals
Antibodies, Neutralizing
/ pharmacology
CX3C Chemokine Receptor 1
/ genetics
Cell Adhesion
Cell Survival
Cells, Cultured
Chemokine CX3CL1
/ antagonists & inhibitors
Dinoprostone
/ metabolism
Disease Models, Animal
Enzyme Inhibitors
/ pharmacology
Epithelial Cells
/ drug effects
Female
Macrophages, Peritoneal
/ drug effects
Mice, Inbred C57BL
Neutrophil Infiltration
Peritonitis
/ enzymology
Phenotype
Prostaglandin-E Synthases
/ antagonists & inhibitors
Up-Regulation
Journal
Cell death & disease
ISSN: 2041-4889
Titre abrégé: Cell Death Dis
Pays: England
ID NLM: 101524092
Informations de publication
Date de publication:
02 02 2021
02 02 2021
Historique:
received:
18
11
2020
accepted:
11
01
2021
revised:
09
01
2021
entrez:
5
2
2021
pubmed:
6
2
2021
medline:
14
9
2021
Statut:
epublish
Résumé
Despite the progress to understand inflammatory reactions, mechanisms causing their resolution remain poorly understood. Prostanoids, especially prostaglandin E
Identifiants
pubmed: 33542207
doi: 10.1038/s41419-021-03423-2
pii: 10.1038/s41419-021-03423-2
pmc: PMC7862376
doi:
Substances chimiques
Antibodies, Neutralizing
0
CX3C Chemokine Receptor 1
0
Chemokine CX3CL1
0
Cx3cl1 protein, mouse
0
Cx3cr1 protein, mouse
0
Enzyme Inhibitors
0
Prostaglandin-E Synthases
EC 5.3.99.3
Ptges protein, mouse
EC 5.3.99.3
Dinoprostone
K7Q1JQR04M
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
135Références
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