Researchers from the Buck Institute report one of the first demonstrations of long - term vision restoration in blind mice by
transplanting photoreceptors derived from human stem cells and blocking the immune response that causes transplanted cells to be rejected by the recipient.
Some groups, including Lanza's, are looking to do just that:
transplant photoreceptor cells.
A team of UK stem cell scientists, led by Dr. Robin Ali from UCL Institute of Ophthalmology in London, has developed a new strategy for repairing the retina by
transplanting photoreceptor cells generated in the laboratory from embryonic stem cells.
Not exact matches
Nevertheless, the outcome may pave the way for
transplants of stem cell — derived eye cells called
photoreceptors, which could dramatically improve vision in people with eye disease if all goes according to plan.
He suspects that
transplanted cells are actually restoring the function of «dormant»
photoreceptors.
A
transplant of fresh RPE tissue could rescue dying
photoreceptors.
These findings have suggested the development stages at which to
transplant cells — for instance,
photoreceptor cells need to be relatively more mature than stem cells, according to Thomas Reh, who studies retinal development at the University of Washington.
There are even efforts underway to
transplant cultured
photoreceptor cells into the retina to replace those lost from advanced disease.
When
transplanted to the subretinal space of mice lacking functional
photoreceptors, human embryonic stem cells directed toward a retinal lineage integrate into the outer nuclear layer, express
photoreceptor markers, and restore a light response as determined by the electroretinogram (ERG)[5].
The team
transplanted stem cell - derived
photoreceptors into another strain of mouse, called CRX null, which is congenitally blind.
Confocal images of P150 dystrophic retina
transplanted with hNPCctx — GDNF and double stained with antibodies against human nuclear antigen (red) and either (A) recoverin, a
photoreceptor and cone bipolar cell marker (green), or (B) protein kinase Cα (PKCα), a bipolar cell marker (green).
(E) P150 dystrophic retina
transplanted with hNPCctx — GDNF and stained with cone arrestin antibody showing morphology of rescued cone
photoreceptors (arrows point to cone pedicles).
Thus,
transplanted hNPCctx have the potential to release multiple growth factors, which may act synergistically to slow
photoreceptor degeneration [62], [63].
Of note, while vision rescue requires preservation of some functional
photoreceptors, the mere presence of
photoreceptor cells in the ONL of
transplanted RCS rats does not assure function [61].
Qualitative examination of the host anatomical response to the presence of hNPCctx or hNPCctx - GDNF revealed substantial preservation of the
photoreceptor outer nuclear layer (ONL) overlying all subretinal donor cells (Figure 5E and F), with
photoreceptor rescue gradually declining outside the distribution of the
transplanted cells (Figure 5E and G).
Conservation of visual acuity in the iPS - RPE
transplanted eyes was associated with the preservation of
photoreceptors in the host outer nuclear layer (ONL — Fig. 7A), identified by the expression of rhodopsin in the outer segments of
photoreceptors (Fig. 7A inset, Dystrophic +
transplant).
The location of
transplanted human cells, their expression profile and ability to phagocytose rod
photoreceptor material was examined in vivo using immunohistochemistry.
Inset shows higher resolution confocal images of
photoreceptor cell nuclear layers (DAPI blue) and rhodopsin expression (red) in the dystrophic control (left inset) and dystrophic with iPS - RPE
transplant (right inset) RCS rat.
Retinal
photoreceptor transplants have been successfully achieved in mice, offering new hope for transplantation - based therapies for...