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Sight
gone, but not necessarily lost?
Newswise — Like all tissues in the body, the
eye needs a healthy blood supply to function
properly. Poorly developed blood vessels can
lead to visual impairment or even blindness.
While many of the molecules involved in
guiding the development of the intricate
blood vessel architecture are known, only
now are we learning how these molecules work
and how they might affect sight.
Reporting in the Oct. 16 issue of Cell,
researchers at the Johns Hopkins School of
Medicine find that when some cells in the
mouse retina are not properly fed by blood
vessels, they can remain alive for many
months and can later recover some or all of
their normal function, suggesting that
similar conditions in people may also be
reversible.
“This finding is intriguing,” says Jeremy
Nathans, M.D., Ph.D., a professor of
molecular biology and genetics, neuroscience
and ophthalmology at Johns Hopkins and a
Howard Hughes Medical Institute
investigator. “It suggests that neurons in
the retina can survive for an extended
period of time even though they have been
functionally silenced.”
Three genes — named Fz4, Ndp and Lrp5 —
previously were suspected to be involved in
blood vessel development in the human
retina. Defects in any of these genes cause
hypovascularization — a lack of sufficient
blood vessels — in the retina. Similarly,
eliminating any of these genes in mice can
lead to hypovascularized retinas.
Mice lacking functional Fz4 have poor blood
vessel growth in the retina and are blind,
but it was not known whether the blood
vessel deficiency was the cause of blindness
or whether the absence of Fz4 leads to some
other defect that causes blindness. The team
found that Fz4 function is required only in
blood vessels, where it senses a signal
produced by the Ndp gene in other retinal
cells.
When the team measured electrical responses
in retinal cells of mice lacking Fz4, they
found a defect in electrical signaling in
the middle layer of the retina — the same
region lacking blood vessels.
The researchers then bathed the Fz4 mutant
retinas in oxygen and nutrients to mimic a
normal blood supply, and measured electrical
signaling in response to light.
They found that when provided with oxygen
and nutrients, the retinas were able to
sense light and generate signals similar to
those generated by normal retinas.
The team
suggests that in the absence of Fz4 the
defective blood vessels provide the retinas
with only enough oxygen and nutrients to
keep the retinal cells alive, but not enough
for them to function normally to send
electrical signals.
“If the human retina responds to a decrease
in blood supply in the same way that the
mouse retina responds, then these results
may have relevance for those patients with
vision loss due to vascular defects,” says
Nathans.
“In particular, these experiments
suggest that if a region of the retina has
been deprived of its normal blood supply,
then completely or partially restoring that
supply may also restore some visual
function, even if this happens weeks or
months later.”
This study was funded by the National Eye
Institute and the Howard Hughes Medical
Institute.
Authors on the paper are Yin Ye, Yanshu
Wang, Hugh Cahill, Tudor Badea, Philip
Smallwood and Nathans of Johns Hopkins, and
Minzhong Yu and Neal Peachey of the Cole Eye
Institute, Cleveland Clinic Foundation.
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