EXPRESSION OF CELL-ADHESION MOLECULES AND VASCULAR ENDOTHELIAL GROWTH-FACTOR IN EXPERIMENTAL CHOROIDAL NEOVASCULARIZATION IN THE RAT

Aims-To investigate the longevity and reproducibility of choroidal neo vascularisation (CNV) induced by krypton laser photocoagulation in the rat. The presence of cell adhesion molecules (CAMs) and vascular endo thelial growth factor (VEGF) during the development of CNV was also st udied. Methods-67 pigmented rats underwent retinal photocoagulation by krypton laser. The eyes were examined by either single or serial fluo rescein angiography at 3 days, 1, 2-3, 4-5, 7-8, and 12 weeks post pho tocoagulation. The expression of CAMs (ICAM-1, E-selectin, and CD44) a nd VEGF post photocoagulation was studied by immunohistochemistry. Res ults-CNV related fluorescein leakage appeared in 46.4% of 766 laser sp ots delivered to the 58 eyes that were tested at 2-3 weeks post treatm ent. The ratio of hyperfluorescent laser sites did not change signific antly at 8 weeks post laser. The number of leaky spots was independent of the total number of lesions delivered to each eye (at 2-3 weeks po st laser 10-15 spots/eye: 44% and 25-30 spots/eye: 49%; t=0.7673; p=0. 3903). Nine eyes were followed by serial angiography between 2 and 12 weeks. The laser spots with fluorescein leakage at 2 weeks (51.5%) rem ained leaky at 12 weeks (51.5%). Histopathologically, macrophage accum ulation peaked at 5 days and CNV was firstly observed at 1 week post p hotocoagulation. ICAM-1, E-selectin, CD44, and VEGF were maximally ind uced at 3-5 days post laser photocoagulation, and were localised to RP E, choroidal vascular endothelial, and inflammatory cells. VEGF was al so detected in intravascular leucocytes at the sites of laser lesions. Conclusions-These studies demonstrated that krypton laser photocoagul ation can be successfully used to produce lesions similar to those of human CNV. The response induced remained present for an extended perio d of time (12 weeks), thus offering a potential model to screen candid ate CNV inhibitory agents. In addition, it is proposed that the expres sion of ICAM-1, E-selectin, CD44, and VEGF before new vessel formation might be linked to the initiation of CNV.