Fibulin-7 C-terminal fragment and its active synthetic peptide suppress choroidal and retinal neovascularization.
Microvasc Res
; 129: 103986, 2020 05.
Article
in En
| MEDLINE
| ID: mdl-32017943
ABSTRACT
Wet age-related macular degeneration (AMD) and diabetic retinopathy are the leading causes of blindness through increased angiogenesis. Although VEGF-neutralizing proteins provide benefit, inconsistent responses indicate a need for new therapies. We previously identified the Fibulin-7 C-terminal fragment (Fbln7-C) as an angiogenesis inhibitor in vitro. Here we show that Fbln7-C inhibits neovascularization in vivo, in both a model of wet AMD involving choroidal neovascularization (CNV) and diabetic retinopathy involving oxygen-induced ischemic retinopathy. Furthermore, a short peptide sequence from Fbln7-C is responsible for the anti-angiogenic properties of Fbln7-C. Our work suggests Fbln7-C as a therapeutic candidate for wet AMD and ischemic retinopathy.
Key words
Full text:
1
Database:
MEDLINE
Main subject:
Peptide Fragments
/
Retinal Vessels
/
Calcium-Binding Proteins
/
Retinal Neovascularization
/
Choroid
/
Choroidal Neovascularization
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Angiogenesis Inhibitors
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Wet Macular Degeneration
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Year:
2020
Type:
Article