ISOFORMS OF PLATELET-DERIVED GROWTH-FACTOR AND ITS RECEPTORS IN EPIRETINAL MEMBRANES - IMMUNOLOCALIZATION TO RETINAL PIGMENTED EPITHELIAL-CELLS

Epiretinal membranes (ERMs) form on the inner surface of the retina in conjunction with various ocular disease processes, but the factors co ntrolling their development are not understood. The predominant cell t ypes involved are retinal pigmented epithelial (RPE) cells and retinal glia. Cultured RPE cells secrete platelet-derived growth factor (PDGF ), which is chemotactic and mitogenic for both RPE cells and retinal g lia and, therefore, could be involved in the development of ERMs. In t he present study, we performed immunohistochemical staining for PDGF A chain (PDGF-A), PDGF B chain (PDGF-B), and both types of PDGF recepto rs (PDGF(r alpha) and PDGF(r beta)) on ERMs associated with various di sease processes. PDGF-A is detected in most ERMs, regardless of the as sociated disease process, and it appears to be localized predominantly in RPE cells, recognized by the presence of pigment and the immunohis tochemical demonstration of some or all of the following RPE-associate d epitopes: class III beta-tubulin, keratin, the 65-kDa microsomal pro tein recognized by the RPE9 antibody, and cellular retinaldehyde-bindi ng protein. PDGF-B is found only in minor subpopulations of cells in a bout half of the ERMs evaluated and, with only occasional exceptions, appears to be localized almost entirely in brood-borne cells found in and around vessels in vascularized ERMs. Both PDGF(r alpha) and PDGF(r beta) are demonstrated in most ERMs with neither isotype consistently predominating: they are found predominantly on RPE cells with many ce lls expressing both receptor types. ERMs with little or no RPE cell co mponent contain little or no PDGF and PDGF receptor, whereas those in which the RPE cell represents the major cell type, have widespread PDG F and PDGF receptor positivity. These findings show that RPE cells in ERMs produce PDGF-A and PDGF(alpha) and PDGF(beta) receptors and sugge st that autocrine and paracrine stimulation with PDGF may be involved in ERM pathogenesis.