Source: Xinhua| 2018-08-16 01:15:40|Editor: yan

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WASHINGTON, Aug. 15 (Xinhua) -- American researchers have restored for the first time vision in mice through activating retinal stem cells, advancing effort toward therapies for retinal degenerative diseases which currently have no cure.

Researchers reported in a study published on Wednesday in the journal Nature that they reversed congenital blindness in mice by changing supportive cells in the retina called Muller glia into rod photoreceptors.

"This is the first report of scientists reprogramming Muller glia to become functional rod photoreceptors in the mammalian retina," said Thomas Greenwell, the program director for retinal neuroscience of the National Eye Institute that funded the study.

Photoreceptors are light-sensitive cells in the retina in the back of the eye that signal the brain when activated. In mammals, including mice and humans, photoreceptors fail to regenerate on their own.

"Rods allow us to see in low light, but they may also help preserve cone photoreceptors, which are important for color 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," said Greenwell.

Muller glia had been found with regenerative potential in zebrafish where they divide in response to injury and turn into photoreceptors and other retinal neurons.

However, from a practical standpoint, it is counterproductive to injure retina first to activate the Muller glia for a person, according to Chen Bo, associate professor of ophthalmology at the Icahn School of Medicine at Mount Sinai.

"We wanted to see if we could program Muller glia to become rod photoreceptors in a living mouse without having to injure its retina," said Chen, the study's lead investigator.

ONE-TWO PUNCH

In the first phase, Chen's team spurred Muller glia in normal mice to divide by injecting their eyes with a gene to turn on a protein called beta-catenin.

Weeks later, they injected the mice's eyes with factors that encouraged the newly divided cells to develop into rod photoreceptors.

The researchers found that the newly formed rod photoreceptors looked structurally no different from real photoreceptors.

In addition, synaptic structures that allow the rods to communicate with other types of neurons within the retina had also formed.

To determine whether the Muller glia-derived rod photoreceptors were functional, they tested the treatment in mice with congenital blindness.

Functionally, they confirmed that the newly formed rods were communicating with other types of retinal neurons across synapses.

Also, light responses recorded from retinal ganglion cells, neurons that carry signals from photoreceptors to the brain, and measurements of brain activity showed that the newly-formed rods were in fact integrating in the visual pathway circuitry.

Chen's lab is planning to see if the technique works on cultured human retinal tissue.