Alterations in lectin binding accompany increased permeability in the dystrophic rat model for proliferative retinopathy.
In the dystrophic Royal College of Surgeons (RCS) rat, migration of vessels from the inner retina into the retinal pigment epithelium (RPE) is associated with neovascular proliferation and formation of vitreo-retinal membranes (VRMs), (Caldwell et al., 1988; Frank and Das, 1988). We studied permeability and luminal membrane glycoconjugates in these vessels using horseradish peroxidase (HRP) and lectin-ferritin (Fe) techniques. RCS and genetic control rats were injected with HRP, their retinas were fixed, incubated in Fe conjugates of wheat germ agglutinin (WGA-Fe) or concanavalin-A (ConA-Fe), reacted to demonstrate HRP, and prepared for electron microscopy. The RPE and VRM vessels in RCS retinas were compared with the normal inner retina and choriocapillaris vessels in RCS and genetic control rats. In both groups inner retinal vessels formed a barrier to HRP, while fenestrated choriocapillaris (CE) vessels were permeable to the tracer. In both of these vascular beds plasma membrane WGA-Fe binding was dense and uniform, while ConA-Fe binding was sparse and patchy. Studies with competitive sugars showed that WGA-Fe binding was primarily to N-acetylglucosamine (NAG) and that ConA-Fe was to mannose. In both RPE and VRM vessels tight junctions appeared intact, but both vessel types were permeable to HRP with the RPE vessels often containing fenestrae and channels. As compared with binding in the inner retina and CE vessels, WGA-Fe binding was lower in VRM vessels and normal in RPE vessels, while ConA-Fe binding was higher in both RPE and VRM vessels. Thus, increased permeability is accompanied by alterations in both NAG and mannose residues in the VRM vessels and with alterations in mannose residues and the presence of fenestrations and channels in the RPE vessels.
Fitzgerald
M E
ME
Dept. of Anatomy and Neurobiology, Univ. TN, Memphis.
Slapnick
S M
SM
Caldwell
R B
RB
D000818:Animals; D001665:Binding Sites; D001667:Binding, Competitive; D002199:Capillary Permeability; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000378:metabolism; D037102:Lectins / Q000378:metabolism*; D008358:Mannose / Q000378:metabolism; D010857:Pigment Epithelium of Eye / Q000098:blood supply / Q000648:ultrastructure; D051381:Rats; D011922:Rats, Mutant Strains; D015861:Retinal Neovascularization / Q000378:metabolism* / Q000473:pathology; D012171:Retinal Vessels / Q000378:metabolism / Q000648:ultrastructure
D037102:Lectins; D008358:Mannose