A primary role for RPE transplants in the inhibition and regression of neovascularization in the RCS rat.
OBJECTIVE
Healthy retinal pigment epithelial (RPE) cell transplants in retinas of postnatal day 27 Royal College of Surgeons (RCS) rat are capable of preventing photoreceptor cell degeneration, inhibiting the degeneration of the retinal vascular bed and the subsequent neovascularization of the RPE that occurs in retinas injected with saline. In the present study, the authors have tested the hypothesis that RPE transplants might also prevent vascularization of the RPE layer in RCS retinas when photoreceptor cells either had just degenerated or, at 3 months, disappeared.


METHODS
Retinas of 3- and 6 month-old RCS rats were injected with either healthy neonatal RPE cells or vehicle and were examined at 6 and 8 months, respectively. These retinas were studied using horseradish peroxidase visualization of the vasculature in retinal wholemount preparations and by light microscopy.


RESULTS
The number of neovascular profiles in wholemount preparations of RCS retinas that had received healthy RPE transplants at 3 months and were analyzed at 6 months were significantly decreased when compared to sham-injected retinas of age-matched RCS rats, 2.09 +/- 0.94 and 15.28 +/- 1.34 profiles per mm2, respectively (P < 0.001). In addition, when comparing retinas transplanted or sham injected at 6 months and examined at 8 months, significantly fewer neovascular profiles were found in the transplant group, 9.32 +/- 1.02 and 15.42 +/- 0.84 profiles per mm2, respectively (P < 0.002).


CONCLUSIONS
These data provide still further evidence for the role of healthy RPE in maintaining the homeostasis of the normal retinal vasculature in the retina of the RCS rat. The relationships between the RPE and the retinal vasculature are important when considering that alterations in the vascularization of the retina play a major role in some of the most sight-debilitating diseases, such as the wet form of age-related macular degeneration and proliferative diabetic retinopathy.
Seaton
A D
AD
Department of Ophthalmology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina.
Sheedlo
H J
HJ
Turner
J E
JE
D000818:Animals; D002469:Cell Separation; D002478:Cells, Cultured; D004195:Disease Models, Animal; D006706:Homeostasis / Q000502:physiology; D006735:Horseradish Peroxidase; D010786:Photoreceptor Cells / Q000473:pathology; D010857:Pigment Epithelium of Eye / Q000502:physiology / Q000637:transplantation*; D051381:Rats; D011922:Rats, Mutant Strains; D012160:Retina / Q000601:surgery / Q000648:ultrastructure; D012162:Retinal Degeneration / Q000473:pathology / Q000517:prevention & control*; D015861:Retinal Neovascularization / Q000473:pathology / Q000517:prevention & control*; D012171:Retinal Vessels / Q000503:physiopathology
D006735:Horseradish Peroxidase