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Increased
Expression of Placenta Growth Factor in Proliferative Diabetic Retinopathy
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Asud Khaliq,
David Foreman, Asif Ahmed, Herbert Weich, Zdenek Gregor, David McLeod, and
Mike Boulton |
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Reproductive
Physiopathology Group, Department of Obstetrics and Gynaecology (AK, AA),
Birmingham Women's Hospital, University of Birmingham, Edgbaston, Birmingham,
and University Department of Ophthalmology (DF, DM. MB), Manchester Royal
Eye Hospital, Manchester, United Kingdom; Department of Gene Expression
(HW), Gesellschaft fur Biotechnologische Forschung, Braunschweig, Germany;
and Moorfields Eye Hospital (ZG), London, United Kingdom |
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Proliferative diabetic
retinopathy is thought to be mediated by the hypoxic regulation of angiogenic
growth factors, in particular the vascular endothelial growth factor (VEGF)
family. The aim of this study was to determine if placental growth factor
(PlGF), a recently identified member of the VEGF family, was expressed in
diabetic eyes undergoing preretinal neovascularization. Rabbit anti-PlGF
antiserum was raised using a 20-amino acid N-terminal sequence to PlGF and
did not cross react with VEGF165. Immunohistochemistry was performed on
specimens of normal retina (n = 8), diabetic retina in the absence (n =
7) and presence (n = 4) of proliferative retinopathy, scatter laser-treated
diabetic retina (n = 7), excised fibrovascular preretinal membranes (n =
12), and nondiabetic fibrocellular epiretinal (n = 7) membranes. PlGF levels
were also determined in vitrectomy specimens from patients with either proliferative
diabetic retinopathy or macular hole. PlGF immunoreactivity was intensely
localized to the endothelial and perivascular regions of newly formed blood
vessels of excised fibrovascular preretinal membranes. Intense localization
of PlGF protein was also observed in superficial retinal vessels in diabetic
retinae adjacent to neovascular preretinal membranes. Localization of PlGF
was weak or absent in diabetic retinae that showed no evidence of neovascular
proliferation. PlGF protein was also absent in normal retinae, in diabetic
retinae that had received extensive treatment with scatter laser photocoagulation,
and in nonvascularized epiretinal membranes. PlGF was present in all diabetic
vitreous samples (mean 103 pg/ml) but nondetectable in control samples.
These results strongly implicate a role for PlGF in the pathogenesis of
proliferative diabetic retinopathy. |
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