January 04, 2005.
GAINESVILLE - Stem cell scientists at the University of Florida announced Monday that they have succeeded in staving off blindness in mice afflicted with a condition similar to one that robs thousands of diabetic Americans of their eyesight each year.
Now the challenge is to see how well that therapy translates from mice to men.
Diabetic retinopathy is the leading cause of blindness in working-age adults, causing 12,000 to 24,000 cases of blindness each year in the United States, according to the American Diabetes Association.
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 cause even more leaks.
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, or stromal-derived factor 1, and retinopathy.
Stromal cells are support cells in bone marrow that help blood cells grow, releasing SDF-1 as a signal to activate the process. UF researchers led by Edward Scott used a common antibody to block the formation of SDF-1 in the eyeballs of mice with simulated retinopathy, putting the brakes on the explosive blood vessel growth that characterizes the condition.
Scott is an associate professor of molecular genetics at the UF Shands Cancer Center and director of the program in stem cell biology and regenerative medicine in the College of Medicine.
"If you get a cut, the body makes SDF-1 at the injury site and the repair cells sniff it out," Scott explained. "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."
In diabetic retinopathy, as new blood vessels continue to grow out of control, damage occurs to the retina, gradually destroying its ability to capture images and eventually leading to blindness.
The researchers assumed that SDF-1 was the key, because it does not break down in the eye and continues to encourage the growth of more blood vessels. They added the protein to the eyeballs of 10 laboratory mice and succeeded in creating a retinopathy-like condition.
Then, as a treatment, scientists injected an SDF-1 antibody directly into the afflicted eyes. The antibody disabled SDF-1's ability to summon stem cells, effectively halting the growth of almost all new blood vessels.
In the next phase of the study, to begin later this month, the approach will be tested in monkeys at Emory University's primate research facility. Support will come from RegenMed, an Alachua-based company founded by Scott and other UF researchers to bring biomedical therapies to market.
If the study in primates is successful, clinical trials in human patients may follow. Scott expects to see positive results.
"The basic technique (of putting an antibody in) is something that has been done for a number of other things," he said. "It should translate fairly well. This is something that can be rapidly adapted and brought to market."
"It would potentially be a treatment option," said Dr. Maria Grant, a professor of pharmacology and therapeutics in UF's College of Medicine who participated in the research. Current therapy for severe diabetic retinopathy uses lasers to destroy parts of retina that are not needed for precise vision in order to improve oxygen delivery to parts that are needed for detailed vision.
"It sounds about as brutal as it is," Scott added. If the results of the current study lead to a new therapy for diabetic retinopathy, he said, the SDF-1 could be injected into the eye as people are being regularly checked for the progression of the disease.
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