SEATTLE, WA — Scientists at the University School of Medicine in Seattle have successfully regenerated cells in the retina of adult mice, raising hopes of new ways to restore sight.

Some body tissues, like our skin, regenerate because of the stem cells that divide into cells that repair damaged tissue. Like mice, human the retinal cells in our eyes cannot regenerate. As a result, retina damage often produces permanent vision loss.

Animals like Zebrafish can regenerate retinal tissue because of cells called Müller glia that harbor a gene, Ascl1, that can prompt retinal tissue to heal once it has been injured.

Led by Tom Reh, a professor of biological structure at the UW School of Medicine, the team studied how this gene could artificially reprogram Müller glia in grown mice. The paper, published in Nature, was written by Nikolas Jorstad, a doctoral student in biological structure in the Department of Pathology.

The gene codes for a type of protein called a transcription factor affect the activity of other genes and have a major effect on cell function. For zebrafish, activating Ascl1 reprograms the glia into stem cells that transform into the cells needed to repair the retina.

Creating a mouse that had a version of the Ascl1 gene in its Müller glia, turning on the gene with an injection of the drug tamoxifen.

The team’s earlier studies showed that the gene’s activation divide the Müller glia into retinal cells called interneurons after an injury to mice retina. Interneurons receive and process signals from the retina's light-detecting cells, rods and the cones, and transmit them to another group of cells that relay the information to the brain.

In their earlier research, the team found that activating the gene worked during the first two weeks after birth alone – the mice could no longer repair their retinas after that period.

Originally, Reh theorized another transcription factor was involved. The team eventually concluded that genes vital to the Müller glia regeneration were being blocked by molecules that bind to chromosomes.

By using a drug that blocks epigenetic regulation called a histone deacetylase inhibitor, Reh and his team activated Ascl1, which allows the Müller glia in adult mice to divide into functioning interneurons.

The team demonstrated that these new interneurons integrate into the existing retina, establish connections with other retinal cells, and react normally to signals from the light-detecting retinal cells.

Reh and his team hope to learn how many factors can activate the Müller glia to regenerate into different types of cells in the retina to develop treatments to repair retinal damage and cure vision loss.

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