Scientists have finally regenerated cells in the retina of adult mice at the University of Washington School of Medicine in Seattle. It is an advanced reverse vision that paves the way novel therapies loss in human. But the results have raised the hope that someday it may be possible to repair retinas damaged by trauma, glaucoma and other eye diseases.

Different tissues in our bodies can heal because they contain stem cells that can divide and differentiate into the type of cells needed to repair damaged tissue. Their efforts are part of the UW Medicine Institute for Stem Cell and Regenerative Medicine.

The cells of our retinas, however, lack this ability to regenerate. As a result, injury to the retina often leads to permanent vision loss. According to researchers at the University of Washington in the US, zebrafish have a remarkable ability to regenerate damaged tissue, including neural tissue like the retina.

This is possible because the zebrafish retina contains cells called Muller glia that harbor a gene that allows them to regenerate. When these cells sense that the retina has been injured, they turn on this gene, called Ascl1. The gene codes for a type of protein called a transcription factor.

It can affect the activity of many other genes and, therefore, have a major effect on cell function. In the case of the zebrafish, activation of Ascl1 essentially reprogrammes the glia into stem cells that can change to become all the cell types needed to repair the retina and restore sight.

The scientists created a mouse that had a version of the Ascl1 gene in its Muller glia. The gene was then turned on with an injection of the drug tamoxifen. Earlier studies by the team had shown that when they activated the gene, the Muller glia would differentiate into retinal cells known as interneurons after an injury to the retina of these mice.

Eventually, they found that genes critical to the Muller glia regeneration were being blocked by molecules that bind to chromosomes. By using a drug that blocks epigenetic regulation called a histone deacetylase inhibitor, activation of Ascl1 allows the Muller glia in adult mice to differentiate into functioning interneurons.

The team hopes to find out if there are other factors that can be activated to allow the Muller glia to regenerate into all the different cell types of the retina. If so, it might be possible to develop treatments that can repair retinal damage, which is responsible for several common causes of vision loss, they said.