Publication: Blood-retina1 barrier breakdown in retinitis pigmentosa:
light and electron microscopic immunolocalization
Authors
Vinores, S.A. ; Küchle, M. ; Derevjanik, N.L. ; Henderer, J.D. ; Mahlow, J. ; Green, W.R. ; Campochiaro, P.A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Macular edema can contribute to visual loss
in the retinitis pigmentosa (RP), but the sites and
mechanism of blood-retina1 barrier (BRB) breakdown
leading to macular edema are not known. An understanding
of the mechanisms involved could lead to the
design of effective pharmacologic therapy to prevent or
minimize macular edema in RP. To investigate this
problem, immunohistochemical staining for albumin was
performed on paraffin sections of 22 normal and 29 RPaffected
eyes. Specimens were graded for extent of
albumin extravasation in different regions of the retina,
optic nerve head, ciliary body, and iris. Electron
microscopic immunocytochemical staining for albumin
was performed on an additional 6 normal and 9 RPaffected
eyes. Two-thirds of the eyes from patients with
RP and no other ocular disorders demonstrated
extravascular albumin in the inner portion of the
posterior retina. This was evident even in the absence of
cystoid macular edema (CME), but eyes that had CME
showed extensive BRB failure. In some cases, passage
of albumin from the choroid to the retina was prevented
even in the absence of the retinal pigment epithelium
(RPE). Electron microscopic immunocytochemistry
revealed that albumin permeated retinal vascular
endothelial cells and RPE cells that showed degenerative
changes in RP.
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