| Abstrakt: |
The first studies showing the potential of retinal cell transplantation to alleviate the progress of blindness in an animal model of retinal disease, the Royal College of Surgeons (RCS) rat, were focused on the fact that in this animal there was a known defect in the retinal pigment epithelium (RPE) that resulted in secondary loss of photoreceptors. It seemed logical to effect cell replacement, by introducing into the subretinal space, normal RPE cells to replace the affected ones. A series of studies showed that the procedure did indeed rescue photoreceptors, presumably by replacing the deficiently functioning cells with ones that function normally. However, RPE cells have many functions, including phagocytosis of outer segments (OS), visual pigment recycling, maintenance of Bruch's membrane, and transport of materials in and out of the retina (1-5).. How many of these several roles are replicated by the grafted cells was not explored in the early studies—indeed very little other than photoreceptor rescue per se was ever measured and, in the absence of suitable labels, it was not even clear how long the donor cells actually survived. Because it was thought that in age-related macular degeneration (AMD), dysfunction, or depletion of RPE cells might be a cause of the photoreceptor loss, the successes in the laboratory were quickly applied to patients with advanced AMD. Irrespective of the causes of AMD, one clear role for RPE cell transplantation was after removing choroidal neovascularization (CNV) membranes that invade the space between Bruch's membrane and the RPE, RPE cells would inevitably be removed too. Repopulation with new cells might correct that deficiency. Results were disappointing: there was suggestion of graft rejection and although little hope of functional improvement might have been expected in the advanced stage patients that formed the subjects of these investigations, attempts to demonstrate visual improvement were equivocal at best. [ABSTRACT FROM AUTHOR] |
