Abstract
Purpose :
Retinal vein occlusion (RVO) can cause significant ocular morbidity including macular edema which can then lead to a reduction of the visual acuity. Anti-vascular endothelial growth factor (anti-VEGF) antibody is now the first choice for eyes with RVO. However, there are some drawbacks such as recurrences of the edema and the progression to the ischemic type of RVO after anti-VEGF antibody therapy. The purpose of this study was to analyze the morphological changes and the expression level of the VEGF molecules after the injection of anti-VEGF antibody in the murine RVO model.
Methods :
The mouse model of RVO was performed by laser photocoagulation after the rose bengal injection at 50mW power, 50 µm size, and 5s duration. The expression level and site of VEGF-related factors and aquaporin4 (AQP4) were investigated by Western blotting and immunostaining after the intravitreal injection of anti-VEGF antibody. The retinal thickness was determined by spectral domain optical coherence tomography and the ocular blood flow was measured by laser speckle flowgraphy
Results :
The administration of the anti-VEGF antibody immediately after the laser irradiation reduced the expression level of VEGF and the degree of downregulation of AQP4. Moreover, an early injection of the anti-VEGF antibody normalized the retinal pathological thickening, and increased the retinal blood flow impairment in all regions of the optic nerve head of the RVO mouse. On the other hand, injection of anti-VEGF antibody 7 days after the laser irradiation reduced these factors compared to that in the control group. In addition, the number of activated astrocytes was increased, and the expression of VEGF around the nonperfusion areas was higher than in the central of nonperfusion areas.
Conclusions :
Our study demonstrated that the partial nonperfusion areas can produce more VEGF than the complete nonperfusion areas in murine RVO model. Moreover, the VEGF inhibition may reduce the degree of retinal edema and nonperfusion areas by the suppression of the downregulation of AQP4 and activated astrocytes.
This is an abstract that was submitted for the 2018 ARVO Annual Meeting, held in Honolulu, Hawaii, April 29 - May 3, 2018.