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Study
Suggests Way to
Replace Diseased Eye Cells
NEW YORK (Reuters Health) - Scientists
in Japan have found a potential way to replace damaged cells in
the eye's retina. Their animal research suggests the technique
could someday prevent blindness from degenerative diseases of
the retina such as macular degeneration and retinitis pigmentosa.
In experiments with rat eye cells, Dr. Masatoshi Haruta of Kyoto
University and colleagues found that some genetic tinkering could
cause cells from the iris to take on new, light-sensitive features
like those of the retina.
The retina is a thin membrane at the back of the eye that captures
images that are then transmitted to the brain through the optic
nerve. Degenerative diseases of the retina are leading causes
of blindness. Once they are damaged, retinal cells cannot regenerate
on their own.
So Haruta's team investigated whether it might be possible to
get cells from the nearby iris to take on the retina's duties.
The surgical removal of part of the iris, they note, is already
an established practice in patients--used, for example, to extract
foreign objects or tumors from the eye.
The researchers took iris cells from rat eyes, then introduced
a gene called Crx that is normally expressed in the photoreceptor,
or light-sensitive, cells of the retina. With the help of Crx,
the iris cells expressed rhodopsin, a substance in the retina
that adapts the eye to changes in light, according to the report
released Monday in the advance online publication of Nature Neuroscience
for December.
In humans, Haruta's team notes, such a technique would allow
doctors to ``feasibly obtain'' a patient's own tissue for use
in retinal regeneration. It might be possible to remove some iris
tissue, coax the cells into taking on retinal qualities, then
transplant them back into a patient's eye.
Although this study is just a beginning, the researchers conclude
that the findings raise ``the possibility that (iris) cells constitute
a potential source of retinal transplantation in patients with
retinal degenerative diseases or damaged retinas.''
SOURCE: Nature Neuroscience 2001;12:10.1038/nn762.
Reference
Source 89
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