Antibodies against retinal pigmented epithelial cells induced RPE cell damage, loss of adhesion, and interphotoreceptor matrix proteins

M. Ayaki, T. Kikuchi, Dhirendra P Singh, S. Suzuki, D. Hamasaki, M. T. Redmont, L. T. Chylack, T. Shinohara

Research output: Contribution to journalArticle

Abstract

Purpose: The primary causes of serous retinal detachment (SRD) remain elusive. One of etiology may involve autoimmune phenomena. We have developed an animal model for SRD. Methods: Animals were immunized with a retinal pigmented epithelial cell (RPE)-specific 65 kDa protein emulsified with complete Freund's adjuvant (CFA). Immunohistochemical, histological, electro-retino-graphic studies and ELISA assay and serum transfer experiment were done in these animals. Results: Rats injected with RPE cell-specific 65 kDa protein emulsified with CFA raised antibodies and developed FPE damage. Serum transfer studies clearly established that the RPE damage vas induced by humoral immunity. The RPE damage resulted in the loss of adhesion proteins and interphotoreceptor matrix (IPM) components including glycoaminoglycan (GAG), integrin, ICAM-1 and VCAM-1. Both RPE cell damage and loss of adhesion and IPM molecules, invariably preceded the detachment of neuro-retina from RPE cells. Conclusions: This experimental animal study of autoimmune RPE damage and SRD offers a model for human SRD. Furthermore, our studies suggest that primary cause of SRD in human is RPE damage induced by humoral autoimmunity.

Original languageEnglish (US)
JournalInvestigative Ophthalmology and Visual Science
Volume37
Issue number3
StatePublished - Feb 15 1996

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Epithelial Cells
Retinal Detachment
Antibodies
Proteins
Freund's Adjuvant
Vascular Cell Adhesion Molecule-1
Intercellular Adhesion Molecule-1
Humoral Immunity
Serum
Autoimmunity
Integrins
Retina
Animal Models
Enzyme-Linked Immunosorbent Assay

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

Cite this

Antibodies against retinal pigmented epithelial cells induced RPE cell damage, loss of adhesion, and interphotoreceptor matrix proteins. / Ayaki, M.; Kikuchi, T.; Singh, Dhirendra P; Suzuki, S.; Hamasaki, D.; Redmont, M. T.; Chylack, L. T.; Shinohara, T.

In: Investigative Ophthalmology and Visual Science, Vol. 37, No. 3, 15.02.1996.

Research output: Contribution to journalArticle

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abstract = "Purpose: The primary causes of serous retinal detachment (SRD) remain elusive. One of etiology may involve autoimmune phenomena. We have developed an animal model for SRD. Methods: Animals were immunized with a retinal pigmented epithelial cell (RPE)-specific 65 kDa protein emulsified with complete Freund's adjuvant (CFA). Immunohistochemical, histological, electro-retino-graphic studies and ELISA assay and serum transfer experiment were done in these animals. Results: Rats injected with RPE cell-specific 65 kDa protein emulsified with CFA raised antibodies and developed FPE damage. Serum transfer studies clearly established that the RPE damage vas induced by humoral immunity. The RPE damage resulted in the loss of adhesion proteins and interphotoreceptor matrix (IPM) components including glycoaminoglycan (GAG), integrin, ICAM-1 and VCAM-1. Both RPE cell damage and loss of adhesion and IPM molecules, invariably preceded the detachment of neuro-retina from RPE cells. Conclusions: This experimental animal study of autoimmune RPE damage and SRD offers a model for human SRD. Furthermore, our studies suggest that primary cause of SRD in human is RPE damage induced by humoral autoimmunity.",
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AU - Ayaki, M.

AU - Kikuchi, T.

AU - Singh, Dhirendra P

AU - Suzuki, S.

AU - Hamasaki, D.

AU - Redmont, M. T.

AU - Chylack, L. T.

AU - Shinohara, T.

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N2 - Purpose: The primary causes of serous retinal detachment (SRD) remain elusive. One of etiology may involve autoimmune phenomena. We have developed an animal model for SRD. Methods: Animals were immunized with a retinal pigmented epithelial cell (RPE)-specific 65 kDa protein emulsified with complete Freund's adjuvant (CFA). Immunohistochemical, histological, electro-retino-graphic studies and ELISA assay and serum transfer experiment were done in these animals. Results: Rats injected with RPE cell-specific 65 kDa protein emulsified with CFA raised antibodies and developed FPE damage. Serum transfer studies clearly established that the RPE damage vas induced by humoral immunity. The RPE damage resulted in the loss of adhesion proteins and interphotoreceptor matrix (IPM) components including glycoaminoglycan (GAG), integrin, ICAM-1 and VCAM-1. Both RPE cell damage and loss of adhesion and IPM molecules, invariably preceded the detachment of neuro-retina from RPE cells. Conclusions: This experimental animal study of autoimmune RPE damage and SRD offers a model for human SRD. Furthermore, our studies suggest that primary cause of SRD in human is RPE damage induced by humoral autoimmunity.

AB - Purpose: The primary causes of serous retinal detachment (SRD) remain elusive. One of etiology may involve autoimmune phenomena. We have developed an animal model for SRD. Methods: Animals were immunized with a retinal pigmented epithelial cell (RPE)-specific 65 kDa protein emulsified with complete Freund's adjuvant (CFA). Immunohistochemical, histological, electro-retino-graphic studies and ELISA assay and serum transfer experiment were done in these animals. Results: Rats injected with RPE cell-specific 65 kDa protein emulsified with CFA raised antibodies and developed FPE damage. Serum transfer studies clearly established that the RPE damage vas induced by humoral immunity. The RPE damage resulted in the loss of adhesion proteins and interphotoreceptor matrix (IPM) components including glycoaminoglycan (GAG), integrin, ICAM-1 and VCAM-1. Both RPE cell damage and loss of adhesion and IPM molecules, invariably preceded the detachment of neuro-retina from RPE cells. Conclusions: This experimental animal study of autoimmune RPE damage and SRD offers a model for human SRD. Furthermore, our studies suggest that primary cause of SRD in human is RPE damage induced by humoral autoimmunity.

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