A team of researchers at the University of Washington School of Medicine in Seattle has found a way to successfully regenerate cells in the retina of adult mice. These results could eventually lead to the treatment of damage caused by injury to the retina, including trauma, glaucoma, and other eye diseases.

The research is published in the journal Nature.

The study was led by Tom Reh, professor of biological structure at the University of Washington School of Medicine. In an interview with The University Network (TUN), he explained the team’s goal. “We hope that someday we will be able to use a similar approach to stimulate the regeneration of new neurons in people who have lost their vision from eye injuries.”

A scrape or a cut on the body naturally heals because our skin contains stem cells that can break up into the type of cells needed to repair damaged tissue. But the cells in our retina lack the ability to naturally heal. So, injury or disease affecting the retina often results in permanent vision loss.

Scientists have discovered that unlike humans, zebrafish have the ability to regenerate damaged tissue in the retina. This is because zebrafish have cells in their retina called Müller glia that possess a gene, Ascl1, which allows them to regenerate. The Ascl1 gene can be reprogrammed into stem cells that create all of the cells needed to naturally repair damage to the eye and repair sight.

In their study, Reh and his team set out to find if they could use the the gene to reprogram Müller glia in adult mice, which, like humans, are unable to naturally repair their retinas.

Previous studies, in which scientists activated the Ascl1 gene, showed that after an injury to the retina the Müller glia in mice would separate into retinal cells called interneurons. Interneurons play an important role in sight because they process signals from light-detecting cells and turn them into another set of cells, which transfer information to the brain.

The initial research seemed successful at first, but the team soon found that activating the gene only worked during the first two weeks after birth. This is because genes essential for Müller glia restoration were being stopped by molecules that bind to chromosomes, a form of epigenetic regulation. This is a common way for cells to block genes from activation.

In an effort to remedy the problems in the previous study, Reh and his team used a drug called histone deacetylase inhibitor, which stops epigenetic regulation.

The results from the new study are promising, but there are still limitations.

“We are so far only able to make a subset of the different types of neurons in the retina, and so at present we would not be able to fully restore vision after a retinal injury,” Reh said. “We don’t know why only some types of neurons are made from the glia, and we are working hard to understand this limitation.”

Reh and his team hope to continue their research to find additional factors that will allow the Müller glia to separate and expand into all types of cells in the retina. If they find such factors, they may be able to resolve the limitations and develop the research to restore human eyesight completely.