TY - JOUR
T1 - Extracellular matrix alterations precede vascularization of the retinal pigment epithelium in dystrophic rats
AU - Caldwell, R. B.
N1 - Copyright:
Copyright 2004 Elsevier B.V., All rights reserved.
PY - 1989
Y1 - 1989
N2 - In Royal College of Surgeons (RCS) rats, the defective retinal pigment epithelium (RPE) fails to phagocytose the shed outer segment membranes, and the photoreceptors degenerate. Following degeneration of the photoreceptors, neovascularization and vitreo-retinal membranes (VRMs) develop. Blood-retinal barrier abnormalities at the level of the RPE suggested that Bruch's membrane extracellular matrix filtration barriers might also be abnormal. To study the progression of RPE cell, extracellular matrix and vascular alterations in the dystrophic retina, we used the cationic tracer polyethyleneimine and electron microscope morphometric techniques. At two weeks in the RCS retina, the RPE and retinal vessels, and their basal laminae, appeared normal. By two months, the RPE was hypertrophic and duplicated in some areas, and flattened in others. The RPE basal lamina was thickened (171% of the control, p < .01), and there were more anionic sites along the RPE basal surface (158% of the control, p < .01). Patches of displaced basal lamina material appeared within the RPE basal infoldings. By four months and later numerous retinal vessels were present within the RPE layer. In addition, cords of migrating RPE cells surrounded presumptive new vessels branching from the RPE layer towards the inner limiting membrane. The RPE-associated vessels exhibited diaphragmed fenestrae and channels, unlike normal retinal vessels, and their basal laminae were marked by anionic sites. These observations of RPE and extracellular matrix changes prior to vascular proliferation, and VRM formation in the dystrophic retina suggest that the RPE-associated extracellular matrix changes may contribute to vascular alterations in the dystrophic retina. A preliminary report of these findings has been presented previously.
AB - In Royal College of Surgeons (RCS) rats, the defective retinal pigment epithelium (RPE) fails to phagocytose the shed outer segment membranes, and the photoreceptors degenerate. Following degeneration of the photoreceptors, neovascularization and vitreo-retinal membranes (VRMs) develop. Blood-retinal barrier abnormalities at the level of the RPE suggested that Bruch's membrane extracellular matrix filtration barriers might also be abnormal. To study the progression of RPE cell, extracellular matrix and vascular alterations in the dystrophic retina, we used the cationic tracer polyethyleneimine and electron microscope morphometric techniques. At two weeks in the RCS retina, the RPE and retinal vessels, and their basal laminae, appeared normal. By two months, the RPE was hypertrophic and duplicated in some areas, and flattened in others. The RPE basal lamina was thickened (171% of the control, p < .01), and there were more anionic sites along the RPE basal surface (158% of the control, p < .01). Patches of displaced basal lamina material appeared within the RPE basal infoldings. By four months and later numerous retinal vessels were present within the RPE layer. In addition, cords of migrating RPE cells surrounded presumptive new vessels branching from the RPE layer towards the inner limiting membrane. The RPE-associated vessels exhibited diaphragmed fenestrae and channels, unlike normal retinal vessels, and their basal laminae were marked by anionic sites. These observations of RPE and extracellular matrix changes prior to vascular proliferation, and VRM formation in the dystrophic retina suggest that the RPE-associated extracellular matrix changes may contribute to vascular alterations in the dystrophic retina. A preliminary report of these findings has been presented previously.
UR - http://www.scopus.com/inward/record.url?scp=0024447033&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0024447033&partnerID=8YFLogxK
M3 - Article
C2 - 2477195
AN - SCOPUS:0024447033
SN - 0271-3683
VL - 8
SP - 907
EP - 921
JO - Current Eye Research
JF - Current Eye Research
IS - 9
ER -