Writing in the current issue of the Journal of Clinical Investigation, researchers describe for the first time the link between a protein known as SDF-1 and retinopathy, a complication of diabetes and the leading cause of blindness in working-age Americans.
Scientists explain how they used a common antibody to block the formation of SDF-1 in the eyeballs of mice with simulated retinopathy, ending the explosive blood vessel growth that characterizes the condition.
Researchers effectively silenced SDF-1's signal to activate normally helpful blood stem cells, which become too much of a good thing within the close confines of the eyeball.
"SDF-1 is the main thing that tells blood stem cells where to go," said Edward Scott, an associate professor of molecular genetics at the UF Shands Cancer Center and director of the Program in Stem Cell Biology and Regenerative Medicine at UF's College of Medicine. "If you get a cut, the body makes SDF-1 at the injury site and the repair cells sniff it out. The concentration of SDF-1 is higher where the cut occurs and it quickly dissipates. But the eye is such a unique place, you've got this bag of jelly -- the vitreous -- that just sits there and it fills up with SDF-1. The SDF-1 doesn't break down. It continues to call the new blood vessels to come that way, causing all the problems."
Diabetic retinopathy causes 12,000 to 24,000 cases of blindness each year, according to the American Diabetes Association. What happens is high blood pressure and blood sugar levels associated with diabetes cause leaks in blood vessels within the eye and hinder the flow of essential chemicals. The eye compensates by growing new blood vessels, which clog the eye and caus
Contact: John Pastor
University of Florida