Inhibition of inflammatory cells delays retinal degeneration in experimental retinal vein occlusion in mice.
Animals
Blood-Retinal Barrier
/ pathology
Cytokines
/ metabolism
Disease Models, Animal
Inflammation
/ metabolism
Macrophages
/ metabolism
Mice
Microglia
/ metabolism
Receptors, Colony-Stimulating Factor
/ antagonists & inhibitors
Retina
/ metabolism
Retinal Degeneration
/ metabolism
Retinal Ganglion Cells
/ pathology
Retinal Vein Occlusion
/ metabolism
blood-retina barrier
inflammation
ischemia
microglia
receptor tyrosine kinase inhibitor
retinal ganglion cell
retinal vein occlusion
Journal
Glia
ISSN: 1098-1136
Titre abrégé: Glia
Pays: United States
ID NLM: 8806785
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
05
09
2018
revised:
09
10
2019
accepted:
10
10
2019
pubmed:
28
10
2019
medline:
20
11
2020
entrez:
26
10
2019
Statut:
ppublish
Résumé
The role of microglia in retinal inflammation is still ambiguous. Branch retinal vein occlusion initiates an inflammatory response whereby resident microglia cells are activated. They trigger infiltration of neutrophils that exacerbate blood-retina barrier damage, regulate postischemic inflammation and irreversible loss of neuroretina. Suppression of microglia-mediated inflammation might bear potential for mitigating functional impairment after retinal vein occlusion (RVO). To test this hypothesis, we depleted microglia by PLX5622 (a selective tyrosine kinase inhibitor that targets the colony-stimulating factor-1 receptor) in fractalkine receptor reporter mice (Cx3cr1
Identifiants
pubmed: 31652020
doi: 10.1002/glia.23739
pmc: PMC7003783
doi:
Substances chimiques
Cytokines
0
Receptors, Colony-Stimulating Factor
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
574-588Informations de copyright
© 2019 The Authors. Glia published by Wiley Periodicals, Inc.
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