Cells within an injured mouse eye can be coaxed into regenerating neurons and those new neurons appear to integrate themselves into the eye’s circuitry, new research shows. The findings potentially open the door to new treatments for eye trauma and retinal disease. The study appears in the July 26 issue of Nature, and was funded in part by the National Eye Institute (NEI), part of the National Institutes of Health.
“The findings are significant because they suggest the feasibility of a novel approach for encouraging regeneration in the mammalian retina, the light sensitive tissue at the back of the eye that dies in many blinding diseases,” said Tom Greenwell, Ph.D., program director at NEI. “Importantly, the investigation also demonstrates that newly generated cells in the mouse retina not only look and behave like neurons, they also wire correctly to the existing neural circuitry at the back of the eye.”
The study’s lead investigator, Tom Reh, Ph.D., and his team at UW Medicine in Seattle, looked to the zebrafish for clues about how to encourage regeneration in the mouse eye. When a zebrafish injures its eye, cells within the eye naturally regenerate, allowing the fish to maintain vision. Mammals lack this regenerative ability.
In studying zebrafish the research team homed in on Müller glia, a type of retinal cell that supports the health and functioning of neighboring neurons, and that also exhibits an innate regenerative ability. Sometimes referred to as the stem cells of the zebrafish eye, Müller glia are the cells from which all other types of retinal cells are regenerated in the fish.
Earlier research from Reh’s lab showed that in newborn mice, Müller glia can be directed to become retinal neurons by activating a transcription factor called Ascl1, which in turn activates a suite of genes involved in regeneration. By the time the mice reach adulthood, however, regions of the genetic code that are targeted by Ascl1 and that are…