By injecting a fused protein called VEGF-TRAP (R1R2) into the eyes or bloodstreams of mice, scientists halted new blood vessel growth in the rodents' eyes and stopped existing blood vessels from leaking. Study results were published recently in the Journal of Cellular Physiology.

VEGF-TRAP was designed to antagonize vascular endothelial growth factor (VEGF), a substance naturally produced in the body that promotes blood vessel formation. Released by the retina (light-sensitive tissue in back of the eye) when normal blood vessels are damaged by disease, VEGF turns on its receptor, igniting a chain reaction that culminates in new blood vessel growth. However, the backup blood vessels are faulty; they leak, bleed and encourage scar tissue that detaches the retina, resulting in severe loss of vision. Such growth is the hallmark of diabetic retinopathy, the leading cause of blindness among young people in developed countries. It's also believed that VEGF contributes to abnormal blood vessel growth from the choroid layer of the eye into the retina, similar to what occurs during the wet or neovascular form of age-related macular degeneration.

VEGF-TRAP contains a portion of two receptors for VEGF, which, hooked together, form a sponge that soaks up VEGF before it causes additional damage. Scientists tested VEGF-TRAP in two groups of laboratory mice. In the first group, which had a rupture of Bruch's membrane (the layer between the retina and the choroid), they injected VEGF-TRAP directly into the rodents' eyes. In a second group of mice genetically engineered to express VEGF in the retina, they gave the mice injections of VEGF-TRAP under the skin.

Mice treated with eit
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Contact: Karen Blum
kblum@jhmi.edu
410-955-1534
Johns Hopkins Medical Institutions
17-Jun-2003