The congenital blindness was reversed by changing supportive cells in the retina called Muller glia into a photoreceptor cell known as rod.
Photoreceptors are light-sensitive cells in the retina in the back of the eye that signal the brain when activated.
However, in mammals including mice and humans, photoreceptors fail to regenerate on their own.
"This is the first report of scientists reprogramming Muller glia to become functional rod photoreceptors in the mammalian retina," said Thomas N. Greenwell, program director at National Eye Institute (NEI) in Marlyland, US.
"Rods allow us to see in low light, but they may also help preserve cone photoreceptors, which are important for colour vision and high visual acuity. Cones tend to die in later-stage eye diseases. If rods can be regenerated from inside the eye, this might be a strategy for treating diseases of the eye that affect photoreceptors," he added.
The findings, reported in the journal Nature, advance efforts toward regenerative therapies for blinding diseases such as age-related macular degeneration and retinitis pigmentosa, the researchers said.
For the study, the team spurred Muller glia in normal mice to divide by injecting their eyes with a gene to turn on a protein called beta-catenin and later, injected the mice's eyes with factors that encouraged the newly divided cells to develop into rod photoreceptors.
They found that the newly formed rod photoreceptors looked structurally no different from real photoreceptors.
Further, the researchers tested the treatment in mice who were born blind. They found that Muller glia-derived rods developed just as effectively as they had in normal mice and were communicating with other types of retinal neurons across synapses.
The researchers also plan to see if the technique works on cultured human retinal tissue.
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