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PubMed1990

Correlation of electroretinographic findings and peripheral retinal nonperfusion in patients with sickle cell retinopathy.

This study examined the relationship between the proportion of peripheral retinal nonperfusion and electroretinogram measures in one untreated eye of 44 patients with sickle cell retinopathy. The proportion of peripheral retinal nonperfusion was derived from fluorescein angiographic frames covering 180 degrees of the temporal periphery. The extent of peripheral retinal capillary nonperfusion was greater in patients with peripheral retinal neovascularization compared with those without neovascularization. Reductions in electroretinogram a- and b-wave amplitudes were found in patients with and without neovascularization. However, such reductions were of greater frequency and magnitude in patients with neovascularization. Electroretinogram abnormalities were restricted to reductions in amplitude; implicit times were generally normal. In terms of the variables of the b-wave luminance-response function, abnormalities were restricted to reductions in the amplitude variable Rmax; values of logK and n were generally within the normal range. Across all patients, there was a significant negative correlation between electroretinogram amplitude measures and capillary nonperfusion, indicating that the electroretinogram provides information about the functional consequences of peripheral capillary nonperfusion in sickle cell retinopathy.

Adolescent↗
PubMed1997

Ocular gene therapy: experimental studies and clinical possibilities.

The Human Genome Project will identify, map and sequence all 50,000-100,000 human genes and will provide the tools to determine the genetic basis of both common and rare diseases. Understanding the genetic basis of human disease will allow for the development of highly specific drugs and for replacement of the altered gene through gene therapy. Gene therapy may also be used to introduce a new function into cells with resulting therapeutic benefit. Genes may be delivered into cells in vitro or in vivo utilizing viral or nonviral vectors. Viral vectors which have been used include retroviruses, adenoviruses, adeno-associated viruses and herpes viruses. Ocular disorders with the greatest potential for benefit of gene therapy at the current time include hereditary ocular diseases, including retinitis pigmentosa, tumors such as retinoblastoma or melanoma, and acquired proliferative and neovascular retinal disorders. We have demonstrated the feasibility of ocular gene therapy in a rabbit model of proliferative vitreoretinopathy, using retroviral vectors containing the herpes simplex virus thymidine kinase 'suicide' gene. Although in vivo transduction efficiency is low, the strong bystander effect results in prominent killing of proliferating cells in this model leading to inhibition of disease. In the future, gene therapy has the potential for the replacement of defective gene products or introduction of new gene products into ocular cells. The selection of appropriate target genes and cells will be critical, as will the development of a methodology for safe, targeted gene transfer.

Animals↗
PubMed2002

Gene therapy in ocular diseases.

Gene therapy is a novel form of drug delivery that enlists the synthetic machinery of the patient's cells to produce a therapeutic agent. Genes may be delivered into cells in vitro or in vivo utilising viral or non-viral vectors. Recent technical advances have led to the demonstration of the molecular basis of various ocular diseases. Ocular disorders with the greatest potential for benefit of gene therapy include hereditary diseases such as retinitis pigmentosa, tumours such as retinoblastoma or melanoma, and acquired proliferative and neovascular retinal disorders. Gene transfer into ocular tissues has been demonstrated with growing functional success and may develop into a new therapeutic tool for clinical ophthalmology in future.

Animals↗
PubMed2003

Transforming growth factor-beta induces expression of vascular endothelial growth factor in human retinal pigment epithelial cells: involvement of mitogen-activated protein kinases.

Vascular endothelial growth factor (VEGF) is a major agent in choroidal and retinal neovascularization, events associated with age-related macular degeneration (AMD) and diabetic retinopathy. Retinal pigment epithelium (RPE), strategically located between retina and choroid, plays a critical role in retinal disorders. We have examined the effects of various growth factors on the expression and secretion of VEGF by human retinal pigment epithelial cell cultures (HRPE). RT-PCR analyses revealed the presence of three isoforms of mRNA corresponding to VEGF 121, 165, and 189 that were up regulated by TGF-beta1. TGF-beta1, beta2, and beta3 were the potent inducers of VEGF secretion by HRPE cells whereas bFGF, PDGF, TGF-alpha, and GM-CSF had no effects. TGF-beta receptor type II antibody significantly reversed induction of VEGF secretion by TGF-beta. In contrast activin, inhibin and BMP, members of TGF-beta super family, had no effects on VEGF expression in HRPE. VEGF mRNA levels and protein secretion induced by TGF-beta were significantly inhibited by SB203580 and U0126, inhibitors of MAP kinases, but not by staurosporine and PDTC, protein kinase C and NF-kappaB pathway inhibitors, respectively. TGF-beta also induced VEGF expression by fibroblasts derived from human choroid of eye. TGF-beta induction of VEGF secretion by RPE and choroid cells may play a significant role in choroidal neovascularization (CNV) in AMD. Since the secretion of VEGF by HRPE is regulated by MAP kinase pathways, MAP kinase inhibitors may have potential use as therapeutic agents for CNV in AMD.

Antibodies↗
PubMed2000

VEGF is major stimulator in model of choroidal neovascularization.

PURPOSE: Vascular endothelial growth factor (VEGF) is upregulated by hypoxia and is a major stimulatory factor for retinal neovascularization in ischemic retinopathies such as diabetic retinopathy. This study sought to determine if VEGF is a stimulatory factor in a murine model of choroidal neovascularization (CNV). METHODS: Mice with laser-induced ruptures in Bruch's membrane were treated with vehicle alone; a drug that inhibits both VEGF and platelet-derived growth factor (PDGF) receptor kinases; a drug that inhibits PDGF, but not VEGF receptor kinase; or genistein, a nonspecific kinase inhibitor. After two weeks, CNV was quantified and compared. RESULTS: Blockade of phosphorylation by VEGF and PDGF receptors caused dramatic, almost complete inhibition of CNV. Genistein also had an inhibitory effect, but less so than the VEGF/PDGF receptor blocker. Blockade of phosphorylation by PDGF receptors, but not VEGF receptors, had no significant effect on CNV. CONCLUSIONS: These data and our previous study, which demonstrated that a kinase inhibitor that blocks VEGF and PDGF receptors and several isoforms of protein kinase C causing dramatic inhibition of CNV, suggest that VEGF signaling plays a critical role in the development of CNV in this model. If safety is established, the effect of inhibiting VEGF receptor kinase activity should be investigated in patients with CNV.

Animals↗
PubMed1978

Ocular neovascularization. The Krill memorial lecture.

The various vascular systems of the eye can undergo new vessel formation. In this presentation, I discuss new vessel growth in the cornea, lens, iris, ciliary body, choroid, retina, and optic nerve head. No single factor can explain all cases of ocular neovascularization; instead there are multiple factors which can affect the various susceptible vessels. Among the known vasculognic factors are: inflammation and its products, a hypoxic retina diffusable factor, the "tumor angiogenic factor," and possibly an aging factor. The different ocular beds possess differing sensitivity to the various vasculogenic stimuli; the iris and choroid being most sensitive and the retina and ciliary body least sensitive to such stimuli. Retinal neovascularization requires both a biochemical factor and a diseased retinal vascular bed for its induction. Ocular neovascularization is a dynamic process which requires a persisting stimulus or else the new vessels tend to regress. The normal eye seems to possess at least two antivasculogenic agents.

Anemia, Sickle Cell↗
PubMed1988

Retinal revascularization following laser photocoagulation treatment for choroidal neovascular membranes.

Retinal revascularization developed within the treatment scar in 7% of patients who had laser photocoagulation treatment for a choroidal neovascular membrane. This revascularization could be mistaken for recurrent choroidal neovascularization because it initially proliferated into a glomerularlike structure and showed dye leakage on angiography. Unlike choroidal neovascularization, these vessels, however, filled entirely from the retinal circulation and stereoscopic angiograms showed them to be located in the inner retina. In the 20 patients who were followed up, the retinal revascularization first appeared approximately four weeks after treatment and persisted for an average of ten weeks. It was associated with dense laser scarring, retinal capillary obliteration, and internal limiting membrane wrinkling, suggesting that heavy initial laser treatment was a predisposing factor for its development. It is important to differentiate retinal revascularization, which has an excellent prognosis and does not require re-treatment, from recurrent choroidal neovascularization, which usually must be treated promptly to avoid loss in visual acuity.

Adult↗
PubMed1987

Effects of hyperbaric, normobaric and hypobaric oxygen supplementation on retinal vessels in newborn rats: a preliminary study.

An experimental study was conducted on eight litters of newborn rats to evaluate the effects of supplemental oxygen administration on the retinal vasculature. The animals and their mothers were kept inside a pressure chamber and treated for the first 5 days of life. On the sixth day, they were removed and kept for five more days under room air and normobaric conditions. Three litters received continuous flow oxygen at 80% at a compression pressure of +81 kPa, one litter oxygen at 80% at a pressure of -39.5 kPa atms and three other litters received oxygen at 80% under normobaric conditions. The eighth litter was treated with room air oxygen at a compression pressure of +81 kPa. A severe retinopathy with marked retinal neovascularization was seen only in the newborn animals of the litters that received oxygen supplementation under normobaric or hypobaric conditions. Retinal vessels showed no pathological changes in the litters treated with hyperbaric normoxia or hyperoxia. It is possible to hypothesize that the prolonged period of oxygen supplementation failed to produce harmful effects on the retinal vasculature because the moderate hyperbarism caused mild retinal and choroidal vasoconstriction thus preventing excessive oxygen transport to the inner retina from the choroid during hyperoxia without inducing structural damage to the retinal tissue.

Animals↗
PubMed1975

Retinal vascular lesions in two patients with prolapsed mitral valve leaflets.

Two patients with retinal vascular lesions had mid-late systolic clicks on cardiac auscultation, suggesting the diagnosis of prolapsed mitral valve. The first patient demonstrated an inferonasal arteriolar branch occlusion secondary to embolization; the second patient had a central vein occlusion with multiple hemorrhages, glial proliferative tissue, and retinal neovascularization. This report describes the association between the prolapsed mitral valve syndrome and retinal vascular lesions.

Arterial Occlusive Diseases↗
PubMed1992

Localized retinal morphology and differential light sensitivity in diabetic retinopathy. Methodology and clinical results.

The thesis presents a technique designed to allow a comparison of retinal function as assessed by computerized perimetry with retinal morphology as seen on photographs of the ocular fundus, including results from the practical application of this technique in the study of diabetic retinopathy. The basis of the technique is an optical algorithm that allows angular distances in the visual field to be transformed to match linear distances on fundus photographs and fluorescein angiograms. The visual field data is superimposed onto the corresponding retinal morphology on the photograph on the basis of two points of reference. The fixation point in the visual field is superimposed onto the foveola on the photograph of the ocular fundus, and the blind spot in the visual field is superimposed onto the optic disc on the photograph. In the practical application of this technique for the study of diabetic retinopathy, visual field scotomata were found corresponding to areas displaying signs of retinal vascular impairment in the form of vascular occlusion, while no relation was found between visual field scotomata and breakdown of the blood-retina barrier as studied on fluorescein angiograms. Furthermore, visual field scotomata were found to correspond to areas peripheral from retinal neovascularizations, a finding supporting the hypothesis that the neovascularizations develop because of stimulation from vasogenic factors released from ischaemic and hypoxic retinal tissue. Visual field scotomata were also found in relation to retinal cotton wool spots. These scotomata were localized, and not accurately extended, which could be expected if the retinal nerve fiber layer had been damaged. Finally, some visual field scotomata could not be related to any visible funduscopic or angiographical morphology. It is concluded that pathological changes in the inner retinal vascular supply may lead to impairment of visual function in diabetic retinopathy, but that also other mechanisms not manifested in a morphologically visible way, are involved. A further investigation of the pathophysiology leading to visual impairment in diabetes mellitus should focus on these unknown factors. A possible approach could be the development of new techniques for studying pathophysiological mechanisms in specific retinal layers, and especially the layers supplied by the external vascular supply to the retina from the choroidal circulation.

Diabetic Retinopathy↗
PubMed1993

Insulin-like growth factor I acts as an angiogenic agent in rabbit cornea and retina: comparative studies with basic fibroblast growth factor.

The release of growth factors from ischaemic retina has been hypothesized as the central stimulus for retinal neovascularization in proliferative diabetic retinopathy. Two of the growth factors implicated are insulin-like growth factor-I and basic fibroblast growth factor. We examined the effect of insulin-like growth factor-I on in vivo neovascularization using the established angiogenic model of the rabbit cornea (n = 30), and also compared the effects of insulin-like growth factor-I and basic fibroblast growth factor using two new in vivo systems. Either supraphysiologic concentrations of each growth factor (600 micrograms) were injected intravitreally into pigmented rabbits (n = 21) or porous polyfluorotetraethylene chambers filled with an emulsion containing collagen and growth factor (500 ng) were placed on the retina surface (n = 8). Our results demonstrate that when insulin-like growth factor-I was implanted together with a slow release carrier into the pocket of the normally avascular cornea, insulin-like growth factor-I (10 micrograms/pellet) induced angiogenesis in all rabbits. This degree of angiogenesis was comparable to that previously shown for basic fibroblast growth factor. For the intravitreal studies, the fibrotic component was greater in the basic fibroblast growth factor injected eyes, whereas the vascular component was accentuated in the eyes injected with insulin-like growth factor-I. Light and electron microscopy demonstrated areas of vascular proliferation in both groups. Porous polyfluorotetraethylene chamber studies with insulin-like growth factor-I and basic fibroblast growth factor demonstrated vascular proliferation in the vicinity of the chamber similar to the intravitreal injected eyes, but to a lesser degree than the injected eyes. Our experiments overall support the angiogenic potential of both insulin-like growth factor-I and basic fibroblast growth factor and support distinct but complimentary roles for each growth factor in the pathogenesis of proliferative diabetic retinopathy.

Animals↗
PubMed1999

Progressive changes in the fluorescein and indocyanine green angiogram in acute idiopathic maculopathy.

AIMS/BACKGROUND: To report progressive changes in the fluorescein and indocyanine green angiograms of a patient with acute idiopathic maculopathy (AIM). METHODS: Over a two-year period, the patient underwent repeated ophthalmoscopic examinations and fluorescein (FA) and indocyanine green (ICG) angiography. RESULTS: The patient presented with subretinal neovascularization in his right eye. He developed recurrences after laser photocoagulation and surgical removal of the neovascular complex. One year later, he experienced a sudden loss of vision in his left eye with a maculopathy consistent with AIM. The maculopathy resolved after two weeks with poor vision. During the acute stage, FA showed lobular hyperfluorescence in the early phase and pooling in the late phase of the angiogram. In the resolved stage of the disease, FA showed irregular window defects and blockage. ICG revealed late hyperfluorescence of the macula in the acute stage. In the resolved stage of the disease, early hypofluorescence was noted in the ICG, which persisted throughout the late phase. CONCLUSION: This patient had poor vision in his right eye as a result of subretinal retinal neovascularization and poor vision in his left eye from a severe form of AIM. FA and ICG differed markedly during the acute and resolved stages of AIM. All cases of idiopathic subretinal neovascularization should be carefully evaluated to exclude AIM as the primary disease.

Acute Disease↗
PubMed1998

Requirement for vascular endothelial growth factor in wound- and inflammation-related corneal neovascularization.

PURPOSE: Vascular endothelial growth factor (VEGF) is required for vascular development and for ischemia-related tumor, iris, and retinal neovascularization. The role of VEGF in inflammatory corneal neovascularization is unknown and was investigated in these studies. METHODS: A rat model was used in which removal of the corneal and limbal epithelium resulted in circumferential neovascularization. Corneal VEGF mRNA levels were quantified with ribonuclease protection assays, and VEGF protein was studied in situ using immunohistochemical analysis. Controlled-release pellets containing anti-VEGF antibodies were implanted into the corneal stroma and were used to determine the requirement for VEGF in corneal neovascularization. RESULTS: VEGF mRNA and protein were induced to high levels after corneal injury and were temporally and spatially correlated with inflammation and neovascularization. VEGF immunoreactivity was localized primarily to the inflammatory cells invading the wounded cornea. The specific inhibition of VEGF bioactivity with neutralizing antibodies potently suppressed corneal neovascularization. CONCLUSIONS: These data are the first to demonstrate that VEGF may be required for inflammatory neovascularization of the rat cornea and to identify VEGF as a functional endogenous corneal angiogenic factor.

Animals↗
PubMed1997

Advanced glycation end products induce expression of vascular endothelial growth factor by retinal Muller cells.

Recent studies have suggested that advanced glycation end products (AGEs) are involved in the development of diabetic complications. To assess the pathogenic role of AGEs and vascular endothelial growth factor (VEGF) in the development of retinal neovascularization in diabetic retinopathy, we investigated the effect of AGEs on induction of VEGF by retinal Muller cells and measured AGE and VEGF concentrations in the vitreous of patients with proliferative diabetic retinopathy (PDR) and nondiabetic patients. The expression of VEGF mRNA and the production of VEGF protein by cultured Muller cells were enhanced by the presence of AGEs. The vitreous concentrations of AGEs and VEGF were both elevated in patients with PDR compared with patients without diabetes (P < 0.01). There was a moderate positive correlation between the levels of crossline and VEGF (r=0.698, P < 0.01). Elevation of AGEs in the vitreous may promote intraocular neovascularization in diabetic retinopathy through production of VEGF from Muller cells.

Aged↗
PubMed1979

Proliferative diabetic retinopathy in patients with defects of platelet function.

A 71-year-old woman had von Willebrand's disease, an inheritable abnormality of platelet activity, and developed diabetic retinal neovascularization. A 59-year-old man had a myeoloproliferative disorder with thrombocythemia but may have had retinal changes before the development of his platelet dysfunction. The occurrence of diabetic proliferative retinopathy in patients with reduced platelet activity suggests that platelet induced microcirculatory abnormalities may not be required for neovascularization.

Aged↗
PubMed2005

Neovascularization in branch retinal vein occlusion combined with arterial insufficiency.

The aim of this study is to elucidate the association of neovascularization in branch retinal vein occlusion (BRVO) combined with major arterial insufficiency (MAI), compared with BRVO alone. The authors retrospectively reviewed the charts, color photographs, and fluorescein angiograms of 304 patients (308 eyes) who had BRVO from 1990 to 2002 at Hanyang University hospital. Patients with BRVO combined with MAI and patients with BRVO alone were differentiated by angiographic appearance. Of the 308 eyes, 12 (3.9%) had neovascularization, all of which were in the 56 eyes of the MAI group for which the neovascularization rate was 21.4%. Neovascularization in BRVO was more strongly associated with the non-perfusion caused by MAI, rather than with the extent of the non-perfusion area that originated from retinal capillary obstruction. MAI is considered as a risk factor for neovascularization and hence could be a prognostic factor.

Adult↗
PubMed2001

Angiostatin inhibits pathological but not physiological retinal angiogenesis.

PURPOSE: Antiangiogenic treatment is a promising new therapy for angiogenesis-dependent diseases. In the current study, the biologic effects on pathologic and physiological angiogenesis in the retina of angiostatin, a very potent angiogenesis inhibitor were determined. In addition, the effects of angiostatin on the growth and development of newborn mice were examined. METHODS: Oxygen-induced retinopathy was induced by subjecting mice postnatal day (P)7 to hyperoxic conditions (5 days) followed by normoxic conditions (relative hypoxia). Mice were treated with angiostatin (intravitreal or systemic). Retinal blood vessels were visualized by fluorescein angiography. Retinal neovascularization was assessed by counting intravitreal endothelial cell nuclei. Growth and organogenesis were determined between P0 and P14. RESULTS: Relative hypoxia resulted in intravitreal proliferation of retinal blood vessels. However, proliferation was inhibited completely by systemic administration of angiostatin without affecting normal retinal vascularization. After intravitreal injection of angiostatin, pathologic proliferation of the retinal blood vessels was impaired by 62%. Neither systemic nor intravitreal treatment impaired the development or growth of organs throughout the body. CONCLUSIONS: Angiostatin inhibits oxygen-induced intravitreal pathologic retinal angiogenesis without affecting the development of physiological retinal vascularization, development, and growth of newborn mice. Therefore, antiangiogenic treatment may be a useful tool in the treatment of proliferative retinopathies.

Angiostatins↗
PubMed1996

The effect of external eye irradiation on choroidal circulation.

BACKGROUND: The effect of external beam radiation therapy (teletherapy) on the choroidal circulation is poorly known. Eyes irradiated with teletherapy represent a good model to study, without confounding factors, the pathophysiologic and clinical aspects of radiation-induced chorioretinal damage. This study used fluorescein and indocyanine green choroidal angiography to investigate the late effects of external eye irradiation on the choroidal circulation. METHODS: Fluorescein angiography and indocyanine green choroidal videoangiography were performed on patients with radiation retinopathy because of external eye irradiation for orbital and paranasal sinus malignancies. Patients were divided into two groups according to the treatment field (anterior unilateral or bilateral). RESULTS: Indocyanine green angiograms showed areas of choriocapillaris hypoperfusion in all eyes-unilateral or bilateral irradiation-affected by radiation retinopathy. Late indocyanine green choroidal staining was found in five eyes (28%) of the patients who received unilateral anterior irradiation. In the same group, nine eyes (52%) had signs of choroidal precapillary occlusion and four eyes (23%) had rubeosis iridis without retinal neovascularization. One case of subfoveal choroidal neovascularization was documented in the bilateral irradiation group. CONCLUSIONS: Radiation side effects are not limited to the retinal vessels but also involve choroidal circulation. The damage to the choroid is primarily vascular, and its clinical aspects depend on the treatment fields. Anterior irradiation may be a critical factor for the appearance of unusual rubeosis iridis and neovascular glaucoma.

Adolescent↗