Irisin Attenuates Pathological Neovascularization in Oxygen-Induced Retinopathy Mice.
Animals
Cells, Cultured
Culture Media, Conditioned
/ pharmacology
Disease Models, Animal
Endothelial Cells
/ metabolism
Fibronectins
Humans
Inflammation
/ pathology
Mice
Mice, Inbred C57BL
NF-kappa B
Neovascularization, Pathologic
/ drug therapy
Oxygen
/ toxicity
Retinal Neovascularization
/ metabolism
Journal
Investigative ophthalmology & visual science
ISSN: 1552-5783
Titre abrégé: Invest Ophthalmol Vis Sci
Pays: United States
ID NLM: 7703701
Informations de publication
Date de publication:
01 06 2022
01 06 2022
Historique:
entrez:
23
6
2022
pubmed:
24
6
2022
medline:
28
6
2022
Statut:
ppublish
Résumé
Abnormal angiogenesis is a defining feature in a couple of ocular neovascular diseases. The application of anti-VEGFA therapy has achieved certain benefits in the clinic, accompanying side effects and poor responsiveness in many patients. The present study investigated the role of irisin in retinal neovascularization. Western blot and quantitative PCR were used to determine irisin expression in the oxygen-induced retinopathy mice model. The pathological angiogenesis and inflammation index were examined after irisin administration. Primary retinal astrocytes were cultured and analyzed for VEGFA expression in vitro. Astrocyte-conditioned medium was collected for transwell assay and tube formation assay in human microvascular endothelial cells-1. Irisin was downregulated in the oxygen-induced retinopathy mice retinae. Additional irisin attenuated pathological angiogenesis, inflammation, and apoptosis in vivo. In vitro, irisin decreased astrocyte VEGFA production, and the conditioned medium suppressed human microvascular endothelial cells-1 migration. Last, irisin inhibited hypoxia-inducible factor-2α, nuclear factor-κB, and pNF-κB (Phospho-Nuclear Factor-κB) expression. Irisin mitigates retinal pathological angiogenesis. Chinese Abstract.
Identifiants
pubmed: 35737379
pii: 2783428
doi: 10.1167/iovs.63.6.21
pmc: PMC9233294
doi:
Substances chimiques
Culture Media, Conditioned
0
FNDC5 protein, mouse
0
Fibronectins
0
NF-kappa B
0
Oxygen
S88TT14065
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
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