Inhibition of choroidal neovascularization by anti-EphB4 monoclonal antibody

The aim of this study was to determine the effect of the EphB4 monoclonal antibody on experimental choroidal neovascularization (CNV) progression. Experimental CNV was established by argon laser photocoagulation. In the experimental group, the EphB4 monoclonal antibody was injected into the vitreous...

Full description

Bibliographic Details
Main Authors: SU, DONGFENG, LI, XIAOQIU, GAO, DIANWEN
Format: Online
Language:English
Published: D.A. Spandidos 2013
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3628074/
Description
Summary:The aim of this study was to determine the effect of the EphB4 monoclonal antibody on experimental choroidal neovascularization (CNV) progression. Experimental CNV was established by argon laser photocoagulation. In the experimental group, the EphB4 monoclonal antibody was injected into the vitreous space in the eye specimens on days 0, 3, 6 and 9 after CNV model establishment. In the control group, an equal amount of balanced salt solution was injected at the same time points. On day 10 after CNV model establishment, fluorescein isothiocyanate-dextran endocardial perfusion and choroidal stretched preparation were conducted, respectively, for the two groups. The CNV area in each light spot and the mean values were determined. Histopathological examination was conducted and the ratio of the maximum thickness of the CNV in each light spot to the surrounding normal choroidal thickness, as well as the mean ratio, were calculated. Choroidal stretched preparation confirmed that the CNV of the experimental group was smaller, whereas the CNV of the control group was wider and larger. Quantitative analysis revealed that CNV in the experimental group was significantly inhibited (t=11.84, P<0.01) and that CNV progression in the experimental group was significantly suppressed (t=7.45, P<0.01). Histopathological examination revealed that CNV in the experimental group was thinner and smaller. Vitreous injection of the EphB4 monoclonal antibody inhibits experimental CNV progression. However, its specific mechanism remains unclear. Endogenous EphrinB2/EphB4 regulates ocular neovascularization and may become a new target in treating CNV diseases.