According to the National Eye Institute, diabetic retinopathy is the most common diabetic eye disease and a leading cause of blindness in American adults. There are roughly 7.7 million adults with the disease in the United States and 93 million worldwide.
While there are currently treatment options for those suffering with diabetic retinopathy, they are very invasive – one requires monthly eye injections – and can mean loss of night vision and peripheral vision.
Julia Busik, an associate professor of physiology in the College of Osteopathic Medicine, is focused on cell therapies to promote blood vessel repair in the eye.
Busik and her research team recently published two papers, one in the journal Stem Cells, and another in PLOS ONE, that describe findings that have implications for new, noninvasive treatment of diabetic retinopathy and possibly other diabetes-related complications.
“The vasculature has a very good capacity for repair,” she says. “If you cut yourself, it’s going to heal. The blood in the vessel will coagulate, a new blood vessel will grow, and you won’t know you had that cut several days later.”
The same thing happens in the retina. The repair is made by cells circulating from the bone marrow. These cells, called progenitor cells, are released to make repairs when damage happens.
Diabetes interferes with the body’s ability to repair itself. In the case of diabetic retinopathy, the progenitor cells have decreased membrane fluidity, making most of the cells unable to squeeze out of the bone marrow into circulation. Even the progenitors that do get released have a decreased ability to find places where repairs are needed.
Busik has found that when a person has diabetes, the progenitor cells produce high levels of an enzyme called acid sphingomyelinase. This leads to certain molecules becoming highly rigid in the membranes and ultimately reduces membrane fluidity.
Working with Gary Blanchard, a professor of chemistry, they measured this fluidity and used animal models to show that blocking the enzyme in the bone marrow of diabetic individuals could protect them from retinal inflammation and damage.
“By just blocking acid sphingomyelinase in the bone marrow cells, we could treat the eye and make it healthy,” she said.
Busik’s challenge going forward is to refine the work. While limiting acid sphingomyelinase appears to be beneficial to the progenitor cells in promoting retinal healing and limiting inflammation, it’s not an enzyme that can be completely blocked, as it could cause other disease complications.
“There are some new delivery mechanisms though that are being developing that could offer better ways to inhibit the enzyme,” she said. “We are working on a few and are also looking at collaborating with other labs.”