Alterations in lectin binding accompany increased permeability in the dystrophic rat model for proliferative retinopathy.

M. E. Fitzgerald, S. M. Slapnick, Ruth B Caldwell

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)409-425
Number of pages17
JournalProgress in Clinical and Biological Research
Volume314
StatePublished - Dec 1 1989
Externally publishedYes

Fingerprint

Ferritins
Retinal Pigment Epithelium
Lectins
Retinal Vessels
Permeability
Horseradish Peroxidase
Retina
Membranes
Mannose
Acetylglucosamine
Glycoconjugates
Tight Junctions
Concanavalin A
Blood Vessels
Electron Microscopy
Cell Membrane
Surgeons

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Alterations in lectin binding accompany increased permeability in the dystrophic rat model for proliferative retinopathy. / Fitzgerald, M. E.; Slapnick, S. M.; Caldwell, Ruth B.

In: Progress in Clinical and Biological Research, Vol. 314, 01.12.1989, p. 409-425.

Research output: Contribution to journalArticle

@article{323086bb2f864f80a0a3d46f5eda1252,
title = "Alterations in lectin binding accompany increased permeability in the dystrophic rat model for proliferative retinopathy.",
abstract = "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.",
author = "Fitzgerald, {M. E.} and Slapnick, {S. M.} and Caldwell, {Ruth B}",
year = "1989",
month = "12",
day = "1",
language = "English (US)",
volume = "314",
pages = "409--425",
journal = "Progress in Clinical and Biological Research",
issn = "0361-7742",
publisher = "John Wiley and Sons Inc.",

}

TY - JOUR

T1 - Alterations in lectin binding accompany increased permeability in the dystrophic rat model for proliferative retinopathy.

AU - Fitzgerald, M. E.

AU - Slapnick, S. M.

AU - Caldwell, Ruth B

PY - 1989/12/1

Y1 - 1989/12/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0024822872&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024822872&partnerID=8YFLogxK

M3 - Article

VL - 314

SP - 409

EP - 425

JO - Progress in Clinical and Biological Research

JF - Progress in Clinical and Biological Research

SN - 0361-7742

ER -