Inhibition of choroidal neovascularization by blocking vascular endothelial growth factor receptor tyrosine kinase

Purpose To investigate the role played by receptors of vascular endothelial growth factors, Flt-1 and KDR/Flk-1, on an experimental model of choroidal neovascularization (CNV). Methods The vascular endothelial growth factor-A (VEGF-A) receptor-specific tyrosine kinase inhibitor SU5416 was administer...

Full description

Saved in:
Bibliographic Details
Published in:Japanese journal of ophthalmology 2008-04, Vol.52 (2), p.91-98
Main Authors: Kami, Junko, Muranaka, Kimimasa, Yanagi, Yasuo, Obata, Ryo, Tamaki, Yasuhiro, Shibuya, Masabumi
Format: Article
Language:English
Subjects:
Angiogenesis Inhibitors - pharmacology
Animals
Apoptosis - drug effects
Capillary Permeability
Choroidal Neovascularization - prevention & control
Disease Models, Animal
Endothelium, Vascular - pathology
Female
Fluorescein Angiography
Immunoenzyme Techniques
In Situ Nick-End Labeling
Indoles - pharmacology
Laboratory Investigation
Medicine
Medicine & Public Health
Mice
Mice, Inbred C57BL
Mice, Knockout
Ophthalmology
Protein-Tyrosine Kinases - antagonists & inhibitors
Pyrroles - pharmacology
Vascular Endothelial Growth Factor A - physiology
Vascular Endothelial Growth Factor Receptor-1 - antagonists & inhibitors
Vascular Endothelial Growth Factor Receptor-2 - antagonists & inhibitors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Purpose To investigate the role played by receptors of vascular endothelial growth factors, Flt-1 and KDR/Flk-1, on an experimental model of choroidal neovascularization (CNV). Methods The vascular endothelial growth factor-A (VEGF-A) receptor-specific tyrosine kinase inhibitor SU5416 was administered to a laser-induced mouse model of CNV. The formation of CNV and the degree of vascular permeability in Flt-1 tyrosine kinase domain-deficient mice were also investigated. Results SU5416 reduced vascularity and vascular endothelial cell proliferation, and promoted endothelial cell apoptosis within CNV. Furthermore, the formation of CNV and the degree of vascular permeability were significantly reduced in Flt-1 tyrosine kinase domain-deficient mice, and this effect was enhanced by the administration of SU5416. Conclusions Both Flt-1 and KDR/Flk-1 have a significant role in CNV formation. Suppression of apoptosis may be involved in the process.
ISSN:0021-5155
1613-2246
DOI:10.1007/s10384-007-0506-6