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 Posted: Fri Nov 28, 2008 5:26 pm Post subject: Retina Regenerated Reh Reports |
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"Some speculate that nerve cells must make stable connections to
survive."
One passage of stable connections is made through the acetylcholine
pathway .. whatever the connection may be .. ?
ScienceDaily (Nov. 24, 2008) — Researchers at the University of
Washington (UW) have reported for the first time that mammals can be
stimulated to regrow inner nerve cells in their damaged retinas.
Located in the back of the eye, the retina>s role in vision is to
convert light into nerve impulses to the brain.
The findings on retina self-repair in mammals will be published the
week of November 24 in the Early Edition of the Proceedings of the
National Academy of Sciences. Other scientists have shown before that
certain retina nerve cells from mice can proliferate in a laboratory
dish. This new report gives evidence that retina cells can be
encouraged to regenerate in living mice.
The UW researchers in the laboratory of Dr. Tom Reh, professor of
biological structure, studied a particular retinal cell called the
Müller glia.
"This type of cell exists in all the retinas of all vertebrates," Reh
said, "so the cellular source for regeneration is present in the human
retina." He added that further studies of the potential of these cells
to regenerate and of methods to re-generate them may lead to new
treatments for vision loss from retina-damaging diseases, like macular
degeneration.
The researchers pointed out the remarkable ability of cold-blooded
vertebrates like fish to regenerate their retinas after damage. Birds,
which are warm-blooded, have some limited ability to regenerate
retinal nerve cells after exposure to nerve toxins. Fish can generate
all types of retinal nerve cells, the researcher said, but chicks
produce only a few types of retinal nerve cell replacements, and few,
if any, receptors for detecting light.
Müller glia cells generally stop dividing after a baby>s eyes pass a
certain developmental stage. In both fish and birds, the researchers
explained, damage to retinal cells prompts the specialized Müller glia
cells to start dividing again and to increase their options by
becoming a more general type of cell called a progenitor cell. These
progenitor cells can then turn into any of several types of
specialized nerve cells.
Compared to birds, the scientist said, mammals have an even more
limited Müller glia cell response to injury. In an injured mouse or
rat retina, the cells may react and become larger, but few start
dividing again.
Because the Müller glia cells appeared to have the potential to regrow
but won>t do so spontaneously after an injury, several groups of
researchers have tried to stimulate them to grow in lab dishes and in
lab animals by injecting cell growth factors or factors that re-
activate certain genes that were silenced after embryonic development.
These studies showed that the Müller glia cells could be artificially
stimulated to start dividing again, and some began to show light-
detecting receptors. However, these studies, the researchers noted,
weren>t able to detect any regenerated inner retina nerve cells,
except when the Müller glia cells were genetically modified with genes
that specifically promote the formation of amacrine cells, which act
as intermediaries in transmitting nerve signals.
"This was puzzling," Reh said, "because in chicks amacrine cells are
the primary retinal cells that are regenerated after injury." To
resolve the discrepancy between what was detected in chicks and not
detected in rodents, the Reh laboratory conducted a systematic
analysis of the response to injury in the mouse retina, and the
effects of specific growth factor stimulation on the proliferation of
Müller glia cells.
The researchers injected a substance into the retina to eliminate
ganglion cells (a type of nerve cell found near the surface of the
retina) and amacrine cells. Then by injecting the eye with epidermal
growth factor (EGF), fibroblast growth factor 1 (FGF1) or a
combination of FGF1 and insulin, they were able to stimulate the
Müller glia cells to re-start their dividing engines and begin to
proliferate across the retina.
The proliferating Müller glia cells first transformed into
unspecialized cells. The researchers were able to detect this
transformation by checking for chemical markers that indicate
progenitor cells. Soon some of these general cells changed into
amacrine cells. The researchers detected their presence by checking
for chemicals produced only by amacrine cells.
Many of the progenitor cells arising from the dividing Müller glia
cells, the researchers observed, died within the first week after
their production. However, those that managed to turn into amacrine
cells survived for at least 30 days.
"It>s not clear why this occurs," the researchers wrote, "but some
speculate that nerve cells have to make stable connections with other
cells to survive."
In addition to Reh, the authors were Mike O. Karl, Susan Hayes,
Branden Nelson, Kristine Tan, and Brian Buckingham, all of the UW
Department of Biological Structure. The research was supported by
postdoctoral fellowships from the German Research Foundation,
ProRetina Travel Grants, National Research Service Awards, and a
National Eye Institute grant from the National Institutes of Health.
Who loves ya.
Tom
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