Researchers have developed new photoreceptor cells on the mouse retina that convert light into electrical signals. Image source: Nathan Devery/Science Source
Some cells in the human eye can repair the damage caused by visually impaired diseases. But so far, scientists have not succeeded in making them work. Now, a research team claims that they have motivated these cells -- called "Muller glial cells --" to regenerate a photoreceptor cell in the eyes of mice. According to a study published in the August 15 issue of the journal Nature in the United Kingdom, these new cells can detect the incoming light and form a network with other cells in the eye to transmit signals to the brain, which is a reversal of some These potential steps in genetic eye diseases and injuries have also brought new hopes for the treatment of blinding diseases such as retinitis pigmentosa. But some people are skeptical about this statement and believe that these signals may come from existing photoreceptor cells rather than newly generated cells.
According to neuroscientist Seth Blackshaw of Johns Hopkins University School of Medicine in Baltimore, Maryland, "No one wants me to be true, but I have serious concerns about this research."
The author of the paper, Professor Chen Bo, professor of neurology and ophthalmology at Mount Sinai College of Medicine in the United States, said that the retina of the zebrafish has a self-repairing function. When the retina is damaged, the "Muller glial cells" can make the nerves of the retina. Cells regenerate, whereas mammalian cells do not have similar regenerative functions. Although the scientific community has been able to activate mammalian "Muller glial cells" by damaging the retina, this method is more harmful to the retina and is not conducive to restoring vision.
To this end, the researchers used gene transfer methods in mouse experiments to cause "Muller glial cells" to divide and develop into sensible rod cells. The newly developed rod cells are structurally indistinguishable from natural rod cells and form synaptic structures that allow them to communicate with other nerve cells in the retina. Experiments have shown that this method can restore the blind mice.
The study was funded by the National Eye Institute of the United States. Thomas Greenwell, director of the Retinal Neuroscience Program, said that this is the first time scientists have reprogrammed Miller's glial cells into functioning rods in the mammalian retina. Rod cells allow people to see things in low light conditions and may help protect cones, which are responsible for distinguishing colors and improving visual acuity.
Chen Bo said that they next plan to use the in vitro culture experiments to study whether the above new method can be used in human retinal tissue.
"No one can create a cell like a photoreceptor like them," said Deborah Otteson, a cell and developmental neurobiologist at the University of Houston's Academy of Ophthalmology in Texas. But she pointed out that even in mice that regenerated the most new rod cells, the density was only 0.2% of the retina of healthy mice. As a result, the treated mice are able to perceive the light, but they cannot recognize the shape or the object.
"They have cracked the first part of the problem, and the problem now is to enlarge it," Otteson said. She said that if researchers can make Miller glial cells produce more photoreceptor cells, this method may one day restore some people who lose their rod cells because of retinal detachment or hereditary retinitis. vision.
Maureen McCall, a neurobiologist at the University of Louisville in Kentucky, said that "a big step forward" in this work was to restore rod cells, but stressed that the research team still needs to prove that rod cell development and function are normal in the diseased eye. - Retinal cells here may not connect and interact properly.
However, Blackshaw saw another explanation for the new findings: in blind mice, existing rod-shaped cells were repaired during surgery, either because they received the corrective genes carried by the virus, or It is because "Miller glial cells" share the right genes with them. In both cases, the brain's visual signal is not derived from newly generated rod-shaped cells, but from the recovery of existing photoreceptor cells. He said the study ignored the chemical labeling technique, which can prove that any functional rod cell is from Miller glial cells.
In this regard, Chen Bo said that he and his team did such a labeling experiment - although not described in the paper, and they have thoroughly proved the origin of new rod cells by several other methods. He also cited a control experiment in which the team transferred the corrective gene to Miller's glial cells without reprogramming. In this case, there is no visual signal in the brain, which means that the existing rod cells are not recovered. (Zhao Xixi)
Related paper information: DOI: 10.1038/s41586-018-0425-3
Chinese Journal of Science (2018-08-21 2nd Edition International)
Source: Chinese Journal of Science
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