Publication: Upregulation of vascular endothelial growth factor in ischemic and non-ischemic human and experimental retinal disease
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Date
1997
Authors
Vinores, S.A. ; Youssri, A.I. ; Luna, J.D. ; Chen, Y.S. ; Bhargave, S. ; Vinores, M.A. ; Schoenfeld, C.L. ; Peng, B. ; Chan, Ch.Ch. ; LaRochele, W. ; 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
Vascular endothelial growth factor (VEGF) is
induced by hypoxia and it has been implicated in the
development of iris and retinal neovascularization (NV)
in ischemic retinopathies in which it has been suggested
that Müller cells are responsible for increased VEGF
production. VEGF, however, is also known to be a
potent mediator of vascular permeability in other tissues
and may perform this function in retina. Immunohistochemical
staining for VEGF was performed on a variety
of human and experimental ischemic and non-ischemic
ocular disorders in which blood retinal barrier (BRB)
breakdown is known to occur to determine if there is an
upregulation of VEGF in these conditions. We found
increased VEGF immunoreactivity in ganglion cells of
rats with oxygen-induced ischemic retinopathy and in
ganglion cells, the inner plexiform layer, and some cells
in the inner nuclear layer of rats with experimental
autoimmune uveoretinitis (EAU), in which there was no
identifiable ischemia or NV. In rats with EAU, VEGF
staining intensity increased from 8 to 11 days after
immunization, coincident with BRB failure. These
results were confirmed using two distinct anti-VEGF
antibodies and by immunoblot and the immunohistochemical
staining was eliminated by pre-incubating the
antibodies with VEGF peptide.
VEGF staining was also increased in the retina and
iris of patients with ischemic retinopathies, such as diabetic retinopathy and retinal vascular occlusive
disease, and in patients with disorders in which retinal
ischemia does not play a major role, such as aphakicl
pseudophakic cystoid macular edema, retinoblastoma,
ocular inflammatory disease or infection, and choroidal
melanoma. VEGF was primarily localized within retinal
neurons and retinal pigmented epithelial cells in these
cases. In addition or in association with its role of
inducing NV, VEGF may contribute to BRB breakdown in a variety of ocular disorders and blockage of VEGF
signaling may help to reduce some types of macular
edema.
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