Scientists at the University of Arkansas for Medical Sciences (UAMS) have discovered how to “reprogram” immune cells to help the eye heal after traumatic injuries and diseases such as diabetic retinopathy.
Findings from research led by Abdel Fouda, PhD, an associate professor in the UAMS College of Medicine’s Department of Pharmacology and Toxicology, were recently published in two peer-reviewed scientific journals: Cell Death & Disease and Cell Death Discovery, both of which are part of Nature, the leading international weekly journal of science.
The findings offer new hope for patients with vision loss caused by ischemia, a condition in which reduced blood flow restricts oxygen and nutrients to tissues. Ischemia can occur with physical trauma to the optic nerve or with such conditions as diabetic retinopathy and central retinal artery occlusion, often called “eye strokes.” All have very few treatment options.
While each study looked at a different eye condition — one focusing on traumatic eye conditions and the other on diabetic retinopathy — researchers found that in both cases, the body’s natural process of clearing away dead cells was hindered by too much of the enzyme HDAC3 in immune cells.
“We found HDAC3 to be increased in immune cells in these retinal diseases, playing a central role in disease progression,” said Fouda, who also works closely with clinicians and researchers in the UAMS Harvey & Bernice Jones Eye Institute. “Our lab is focused on understanding how the eye’s own immune system can be turned from a source of inflammation into a dedicated repair crew. We have found that by targeting specific molecular switches, we can help the eye ‘clean up’ damage and even start to regrow lost vital nerve connections.”
His team discovered that a protein called CD5L acts as a master regulator in the cell cleanup process, and that by increasing the amount of CD5L, immune cells clear debris more effectively, protecting delicate eye tissues.
The second study addressed traumatic optic neuropathy, which can occur after a severe head or facial injury and often leads to permanent blindness. By blocking the HDAC3 enzyme in certain immune cells, the UAMS team created an environment that encourages nerves to regrow. In laboratory models, Fouda said, this approach saved nerve cells and improved their connection to the brain, suggesting a restoration of visual function.