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Results for “Retinal Neovascularization”

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At least 163 records · Page 9Linked to original sources
PubMed2006

[Retinal neovascularization in a traumatic microhyphema].

CLINICAL CASE: This is a case of retinal ischaemia with subsequent neovascularization, in a 13 year-old boy who sustained a traumatic hyphema after blunt trauma. DISCUSSION: Hyphemas can occur after blunt trauma, intraocular surgery, spontaneously and in association with the use of substances that alter platelet or thrombin function (aspirin, ethanol). Associated injuries are traumatic anterior uveitis, iridodialysis, optic atrophy, secondary hemorrhage and a traumatic cataract. This case illustrates the formation of retinal neovascularization in association with a microhyphema and the need for careful and prolonged ophthalmological examination in this clinical context.

Adolescent↗
PubMed1986

Idiopathic sub-retinal neovascular membranes in the macula (hemorrhagic macular choroidopathy of young adults). Clinical report and effectiveness of laser treatment.

Twenty-six patients with idiopathic sub-retinal neovascular membranes (INVMs) located within the posterior pole were examined. Clinical and fluorescein angiographic features of these patients are described. Follow-up ranged from 2 to 96 months (mean 16.5 months). Laser treatment was performed according to the location of the neovascular membrane: 7 out of 9 eyes (77%) increased their final visual acuity or stabilized after Argon blue-green laser photocoagulation (INVMs further than 200 microns from the center of the fovea). Krypton red light laser treatment was performed in 13 eyes with juxta-foveal and sub-foveal INVMs: following treatment 10 eyes (77%) improved by 2 or more Snellen lines or maintained their pre-treatment visual acuity. Because of the fact that the Krypton laser was not yet available, 5 patients were not treated: all of them had sub-foveal (3) or juxta-foveal INVMs (2). The natural history of 4 cases (80%) showed an increase in the final visual acuity in 3 eyes and a steady state in one eye. Pathogenesis and treatment outcome of the disease are finally discussed.

Adolescent↗
PubMed2002

Loss of p53 compensates for alpha v-integrin function in retinal neovascularization.

alpha(v)-Integrin antagonists block neovascularization in various species, whereas 20% of alpha(v)-integrin null mice are born with many normal looking blood vessels. Given that blockade of alpha(v)-integrins during angiogenesis induces p53 activity, we utilized p53 null mice to elucidate whether loss of p53 can compensate for alpha(v)-integrin function in neovascularization of the retina. Murine retinal vascularization was inhibited by systemic administration of an alpha(v)-integrin antagonist. In contrast, mice lacking p53 were refractory to this treatment, indicating that neovascularization in normal mice depends on alpha(v)-integrin-mediated suppression of p53. Blockade of alpha(v)-integrins during neovascularization resulted in an induction of p21(CIP1) in wild type and, surprisingly, in p53 null retinas, indicating that alpha(v)-integrin ligation regulates p21(CIP1) levels in a p53-independent manner. In conclusion, we demonstrate for the first time an in vivo intracellular mechanism for compensation of integrin function and that p53 and alpha(v)-integrins act in concert during retinal neovascularization.

Animals↗
PubMed1993

The effects of intravitreal triamcinolone acetonide on experimental pre-retinal neovascularization.

Corticosteroids, alone or in combination with other drugs, have been shown to inhibit angiogenesis. The purpose of this study was to evaluate the efficacy of triamcinolone acetonide in a new model of preretinal neovascularization. Rabbit eyes were treated with intravitreal triamcinolone acetonide 24 h before partial liquefaction of the posterior vitreous with hyaluronidase and injection of 250,000 homologous tissue-cultured dermal fibroblasts. Triamcinolone acetonide effectively inhibited new vessel growth in treated eyes. Only 14% of the treated eyes developed new blood vessels compared to 100% of sham-injected control eyes (P < 0.001). These results suggest that intravitreal triamcinolone acetonide might be effective in inhibiting new vessel growth in patients with inflammatory retinal neovascularization, such as that associated with sarcoidosis or other uveitic syndromes.

Animals↗
PubMed1979

Peripheral retinal neovascularization in rheumatic fever.

During a two-year period, a 15-year-old boy had three major manifestations of rheumatic fever, ie, chorea, rash, and carditis. Following the acute carditis, peripheral retinal neovascularization appeared in the left eye. Associated transient hemiparesis suggests that emboli may account for the retinal vascular occlusion. Rheumatic fever should be considered in the medical survey of patients who have retinal new vessels of obscure origin.

Adolescent↗
PubMed1989

Peripheral retinal neovascularization in birdshot retinochoroidopathy.

A 69-year-old black woman had ocular findings consistent with birdshot retinochoroidopathy; these included cream-colored depigmented spots at the level of the retinal pigment epithelium and vitreitis. She also had peripheral retinal neovascularization with localized vitreous hemorrhage. There were no laboratory or systemic findings consistent with other disease entities.

Aged↗
PubMed1998

Lipid hydroperoxide stimulates retinal neovascularization in rabbit retina through expression of tumor necrosis factor-alpha, vascular endothelial growth factor and platelet-derived growth factor.

To test the hypothesis that oxidative damage associated with tissue hypoxia plays a role in neovascularization, a lipid hydroperoxide (LHP) was injected into the vitreous of rabbits. Single injections of LHP (50-600 microg) caused a sustained retinal neovascularization visualized clinically by ophthalmoscopy and confirmed by microscopy. Vasodilators, i.e. histamine and nitric oxide, peaked at 6h and 7 days, respectively. The levels of both tumor necrosis factor-alpha and interleukin-1alpha peaked at 12h and dropped to basal levels by 24h. Expression of vascular endothelial growth factor (VEGF) and transforming growth factor-beta peaked at 24h and were sustained throughout the following 3 weeks, and platelet-derived growth factor was also elevated throughout the same period. Upregulation of these five angiogenic cytokines, but not basic fibroblast growth factor, occurred prior to the appearance of neovascularization. Leakage of fluorescein at the tips of new vessels was demonstrated by fluorescein angiography. Linoleic hydroperoxide induced neovascularization, but saturated or unsaturated native C-18 fatty acids had no effect. The cascade of multiple, angiogenic cytokines induced by LHP may interact to promote sustained neovascularization.

Journal Article↗
PubMed1999

Regulation of vascular endothelial growth factor-dependent retinal neovascularization by insulin-like growth factor-1 receptor.

Although insulin-like growth factor 1 (IGF-1) has been associated with retinopathy, proof of a direct relationship has been lacking. Here we show that an IGF-1 receptor antagonist suppresses retinal neovascularization in vivo, and infer that interactions between IGF-1 and the IGF-1 receptor are necessary for induction of maximal neovascularization by vascular endothelial growth factor (VEGF). IGF-1 receptor regulation of VEGF action is mediated at least in part through control of VEGF activation of p44/42 mitogen-activated protein kinase, establishing a hierarchical relationship between IGF-1 and VEGF receptors. These findings establish an essential role for IGF-1 in angiogenesis and demonstrate a new target for control of retinopathy. They also explain why diabetic retinopathy initially increases with the onset of insulin treatment. IGF-1 levels, low in untreated diabetes, rise with insulin therapy, permitting VEGF-induced retinopathy.

Animals↗
PubMedDate not supplied

The interaction between the renin-angiotensin system and vascular endothelial growth factor in the pathogenesis of retinal neovascularization in diabetes.

Despite the use of laser photocoagulation and knowledge of the beneficial effects of good glycaemic control, visual loss due to diabetic retinopathy remains the commonest cause of blindness in the working population. This visual loss is principally the result of proliferative diabetic retinopathy and macular oedema. The processes by which diabetes mellitus results in retinopathy are incompletely understood, but recent evidence has suggested a pathogenetic role for the renin-angiotensin system (RAS) and vascular endothelial growth factor (VEGF) in the eye in response to chronic hyperglycaemia. This review will explore evidence of a local RAS in the eye, the involvement of VEGF in diabetic retinopathy and the interaction between the RAS and VEGF in the pathogenesis of retinal neovascularization.

Animals↗
PubMedDate not supplied

Deficiency of neuropilin 2 suppresses VEGF-induced retinal neovascularization.

Vascular endothelial growth factor (VEGF) plays a central role in the development of ocular neovascularization (NV) and is an excellent target for therapeutic intervention. VEGF acts through several receptors, including VEGF receptor 1, VEGF receptor 2, neuropilin-1 (Npn1), and Npn2, but the exact role of these receptors in the development of retinal NV is unknown. In this study, we investigated the expression of npn2 mRNA during new blood vessel growth in the retina and used npn2 knockout mice to assess the impact of deficiency of Npn2 on retinal NV. The level of npn2 mRNA in the retina increased during retinal vascular development, after exposure to hyperoxia, and after the onset of retinal ischemia. Immunohistochemistry showed colocalization of Npn2 with a vascular marker in retinal NV. Compared with littermate controls, mice deficient in Npn2 had significantly less ischemia-induced retinal NV and very little subretinal NV due to expression of a Vegf transgene. These data suggest that Npn2 facilitates VEGF-induced retinal NV and may constitute a useful target for therapeutic intervention in ocular diseases complicated by NV.

Animals↗
PubMed1979

Talc emboli and retinal neovascularization in a drug abuser.

A 38-year-old male drug abuser had multiple emboli in the retinal circulation of the posterior pole of both eyes. He showed widespread peripheral retinal capillary nonperfusion and neovascular proliferation at the junction of perfused and nonperfused retina. The emboli were considered to be talc particles from the intravenous administration of suspensions of oral medications. The presumed mechanism of development of neovascularization in this case was the filtering out of the particles by the retinal vasculature with vaso-occlusion, ischemia and subsequent retinal neovascularization.

Adult↗
PubMed1975

Peripheral retinal neovascularization in sarcoidosis.

Three black patients with peripheral retinal sea fan neovascularization were found to have sarcoidosis. The periphlebitic process may be the cause of stasis, hypoxia, and a secondary vasoproliferative stimulus. We noted the peculiar finding of a vessel passing through the neovascular tissue into the peripheral retina. This feature may help in the differential diagnosis.

Adult↗
PubMed2003

Retinal neovascular markers in retinopathy of prematurity: aetiological implications.

AIM: (1) To determine if expression of the blood-tissue barrier associated glucose transporter GLUT1 is preserved by the neovasculature of retinopathy of prematurity (ROP), in contrast with the reported loss of GLUT1 expression in preretinal vessels of proliferative diabetic retinopathy. (2) To compare the vascular immunophenotype of ROP to juvenile haemangioma, another perinatal neovascular disorder that has recently been shown to express placental type vascular antigens, including GLUT1 and Lewis Y antigen. METHODS: A retrospective case report was carried out. Immunoreactivities for GLUT1 and Lewis Y antigen were assessed in a human eye with stage 3 ROP and compared with those in a control (paediatric) eye. The presence or absence of endothelial GLUT1 and Lewis Y immunoreactivity was determined in preretinal and intraretinal vessels. RESULTS: Immunoreactivity was positive for GLUT1 and negative for Lewis Y in the intraretinal and preretinal neovasculature of the ROP affected eye and in the normal retinal vessels of the control eye. CONCLUSIONS: Retention of immunoreactivity for GLUT1 distinguishes ROP from proliferative diabetic retinopathy. Furthermore, absence of Lewis Y antigen co-expression distinguishes ROP from juvenile haemangioma, a perinatal form of GLUT1 positive neovascularisation that has recently been linked to placental vasculature.

Biomarkers↗
PubMed2001

Intravitreal VEGF and bFGF produce florid retinal neovascularization and hemorrhage in the rabbit.

PURPOSE: Vascular endothelial growth factor (VEGF) causes widespread retinal vascular dilation, produces breakdown of the blood-retinal barrier, and is implicated in ocular neovascularization (NV). Basic fibroblast growth factor (bFGF) also has been implicated in the production of ocular NV. This study was performed to investigate the ability of simultaneous sustained intravitreal release of both VEGF and bFGF to induce robust retinal NV in the rabbit. METHODS: Intravitreal implantation of sustained-release Hydron polymeric pellets containing both 20 microg of VEGF and 20 microg of bFGF was performed on adult male Dutch belted rabbits. In other animals either 20 microg or 50 microg bFGF-containing pellets was implanted intravitreally; also, either 20 microg VEGF or 50 microg VEGF-containing pellets was implanted. Control rabbits received either blank polymeric pellets or a pellet containing 30 microg bovine serum albumin. Eyes were examined by indirect ophthalmoscopy after surgery at 24 hrs, 48 hrs, 4 days, 7 days, 14 days, 21 days, and 28 days. Findings were documented by color fundus photography and fluorescein angiography (FA). Eyes were enucleated and prepared for histologic analysis at 28 days following intravitreal implantation of the VEGF/bFGF-containing pellets. RESULTS: In all eyes implanted with VEGF/bFGF pellets, dilation and tortuosity of existing blood vessels were observed within 48 hrs after pellet implantation. The progression of retinal vascular changes was rapid and occurred over the entire optic disk and medullary rays between 4 and 7 days. Hemorrhage occurred as early as 14 days after VEGF/bFGF pellet implantation. In eyes with massive hemorrhage, total traction retinal detachment developed after the second week. The presence of abnormal tissues at the vitreo-retinal interface within 28 days was demonstrated by light microscopy while FA showed profuse leakage of dye from anomalous vessels within the first week. Neither bFGF-exposed eyes nor control eyes showed any vascular changes. Eyes that received only VEGF-containing pellets exhibited tortuosity of existing vessels, but neither hemorrhaging nor retinal detachment occurred. CONCLUSIONS: These results demonstrate that retinal vascular changes leading to hemorrhaging is produced rapidly in the rabbit by simultaneous intravitreal release of both VEGF and bFGF. Understanding how these growth factors induce retinal NV may suggest novel therapeutic treatment strategies.

Animals↗