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Results for “Retinal Neovascularization”

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At least 973 records · Page 54Linked to original sources
PubMed1992

Genetic linkage of autosomal dominant neovascular inflammatory vitreoretinopathy to chromosome 11q13.

Autosomal dominant neovascular inflammatory vitreoretinopathy (ADNIV) is an inherited eye disease characterized by retinal and iris neovascularization, abnormal retinal pigmentation, anterior chamber and vitreous inflammation, cystoid macular edema, vitreous hemorrhage, and traction retinal detachment. Some of these clinical features are shared by more common, potentially blinding, conditions including diabetic retinopathy, uveitis, and retinitis pigmentosa. Elucidation of the molecular pathogenesis of ADNIV has the potential to provide insight into the mechanisms of these common disorders. One hundred and sixteen members of an eight generation family affected with ADNIV were examined. A combination of slit lamp biomicroscopy, ophthalmoscopy, and electroretinography was used to establish the diagnosis and 34 family members were found to be affected. Blood samples were obtained from thirty-three of these individuals and nine spouses and used for chromosome linkage analysis with denaturing gradient gel and short tandem repeat polymorphisms. Two markers that map to chromosome 11q13 were found to be significantly linked to the ADNIV phenotype. There were no recombinants between the disease phenotype and marker D11S527 and multipoint analysis yielded a maximum LOD score of 11.9 centered on this marker.

Adult↗
PubMed1998

Expression of vascular endothelial growth factor and its receptor, KDR, following retinal ischemia-reperfusion injury in the rat.

PURPOSE: There is considerable evidence that vascular endothelial growth factor (VEGF) mediates ocular neovascularization in retinal vascular diseases. We investigated the time-dependent changes in the expression of VEGF and its receptor KDR/ Flk in a transient retinal ischemia-reperfusion injury model. METHODS: Transient retinal ischemia was induced by increasing the intraocular pressure in albino rats eyes for 45 min. In situ hybridization was used to identify the retinal cells synthesizing VEGF mRNA and KDR mRNA at various times following reperfusion. Immunohistochemical analysis was also carried out to detect VEGF immunoreactivity. RESULTS: In the control, non-ischemic retinas, signals for VEGF mRNA and KDR mRNA were observed in the cells of the ganglion cell layer. Immunoreactivity to VEGF was also found in the nerve fiber layer, the ganglion cell layer, and the retinal pigment epithelial (RPE) cell layer. Immediately and 6 h after reperfusion, VEGF and KDR mRNA expression was markedly decreased, but recovered by 24 h to the levels observed in normal retinas. Immunoreactivity for VEGF was also decreased immediately and 6 h after reperfusion, and was detected in the endothelial cells of the retinal vessels after 24 h. Immunoreactivity to VEGF recovered by 48 h after reperfusion. CONCLUSIONS: The hybridization pattern of VEGF and KDR mRNA in the ganglion cell layer strongly suggests that the ganglion cells are the major source of this growth factor. The decrease of VEGF mRNA, KDR/Flk mRNA and VEGF protein levels after ischemia and recovery after reperfusion suggest that transient hypoxia might mediate short-term down-regulation of VEGF and KDR mRNA.

Animals↗
PubMed1992

[Selective occlusion of ocular neovascularization by photodynamic therapy].

Photodynamic therapy (PDT) has successfully been used to induce vascular occlusion via endothelial damage and subsequent thrombosis. To increase the selective of this method for neovascularizations, characteristics in the ultrastructure of the proliferative vessel wall allow physiological vessels to be spared and predominantly neovascularizations to be occluded: (a) Due to the disturbance of the blood-retina barrier, free dye molecules accumulate within the vascular wall. Using a dye with prolonged retention, such as phthalocyanine (CASPc), it is possible to thrombose neovascularizations 24 h post injection while leaving the physiological vasculature of the anterior segment of the rabbit eye unaffected. (b) Proliferating endothelial cells express high numbers of low-density lipoprotein (LDL) receptors. Chlorin e6 (Ce6), a potent photosensitizer, is covalently bound to LDL. Intravascularly, ce6-LDL complexes selectively label neovascular walls. Since ce6-LDL is incorporated intracellular into enzymatically active lysosomes, photothrombosis is effectively achieved at low drug and light doses in vivo. In addition, the induced damage is spatially confined to the inner vascular lining. We conclude that carrier-mediated PDT may offer a new and sensitive approach for selective treatment of intraocular neovascularizations.

Animals↗
PubMed1999

VHL gene deletion and enhanced VEGF gene expression detected in the stromal cells of retinal angioma.

OBJECTIVE: Retinal angioma frequently occurs in von Hippel-Lindau (VHL) disease. However, VHL gene alterations have not been documented in retinal angiomas. METHODS: Using tissue microdissection and polymerase chain reaction amplification, we have analyzed 7 retinal angiomas associated with VHL disease for loss of heterozygosity of the VHL gene. In addition, vascular endothelial growth factor expression was evaluated in these tumors by immunohistochemistry and in situ hybridization. RESULTS: All 6 informative retinal angiomas showed loss of heterozygosity of the VHL gene. Loss of heterozygosity was detected in vacuolated "stromal" cells, but not in vascular cells or reactive glial tissue. Vascular endothelial growth factor protein and messenger RNA were also present in vacuolated "stromal" cells. CONCLUSIONS: These findings suggest that vacuolated "stromal" cells represent the true neoplastic component in retinal angioma. These cells express vascular endothelial growth factor and therefore may be responsible for abundant neovascularization of retinal angioma.

Adult↗
PubMed1993

Different determinants of neovascularization on the optic disc and on the retina in patients with severe nonproliferative diabetic retinopathy.

Almost all patients with type I and many with type II diabetes develop proliferative retinopathy. This entity consists of two components: new blood vessels on the optic disc (NVD), which frequently lead to visual loss, and new blood vessels elsewhere on the retina (NVE), which do not pose such a serious threat to vision. This study examined determinants of neovascularization specifically on the optic disc in eyes with severe nonproliferative retinopathy. The study eyes were under surveillance as the untreated control eyes of participants in the Diabetic Retinopathy Study. During the 5-year follow-up period, NVE developed in almost all of the eyes, whereas the cumulative incidence of NVD in these same eyes was 64% and varied according to several factors. The risk of NVD in a study eye was increased if the contralateral treated eye had NVD rather than NVE or severe nonproliferative retinopathy (odds ratio [OR], 6.1; P < .0001). It was also increased if the study eye had, at the baseline examination, soft exudates and intraretinal microvascular abnormalities (OR, 5.7; P = .002) or soft exudates alone (OR, 4.0; P = .04). Nephropathy and poor glycemic control were each associated with a two-fold increase in risk but neither was statistically significant. Eyes of individuals over 40 years of age were protected from the development of NVD (OR, 0.5; P < .05). The findings of this study support the hypothesis that, in patients with diabetes, the development of NVD is determined by different factors than the development of NVE.

Adolescent↗
PubMed2003

[Molecular mechanisms of vasculogenesis and angiogenesis. What regulates vascular growth?].

The basic mechanisms governing how endothelial cells, periendothelial cells, matrix molecules and blood constituents interact with each other are discussed. The many insights gained from this basic knowledge are being extended to further understand physiological and pathological features of vascular sprouting and maintenance. Understanding these basic principles that drive angiogenesis and vasculogenesis will lead to a more specific therapy of many disorders in ophthalmology and other fields, such as arteriosclerosis, tumor growth, myocardial ischemia and tissue repair.

Adult↗
PubMed1990

[Progression of diabetic retinopathy following cataract extraction].

A progression of diabetic retinopathy (DR) has been noted following cataract surgery. The retrospective study reported here covered 219 eyes of diabetic patients on which cataract surgery was performed: in 122 cases with intracapsular cataract extraction (ICCE; Group A) without implantation of an intraocular lens (IOL), and in 97 cases with extracapsular cataract extraction and implantation of an intraocular lens (ECCE + IOL; Group B). The existence of diabetic retinopathy was established preoperatively, enabling the population to be divided into subgroups without DR (Groups A1 and B1) and with DR (Groups A2 and B2). Progression of DR was observed in 18% of the eyes in Group A, as opposed to 9.3% of those in Group B (P less than 0.05). Progression to background retinopathy was observed in 10% of the cases in Group A and in 1.3% of the cases in Group B (P less than 0.025). A deterioration was also observed in 33% of the cases in Group A2 and 40% of those in Group B2. Maculopathy progressed in 23% of the cases in Group A2 and 30% of those in Group B2. Rubeosis iridis occurred in 9% of the cases in Group A2 and 5% of those in Group B2. Vitreous hemorrhage following ICCE occurred in 12% of the cases in Group A2. As regards the incidence of neovascular glaucoma and vitreous hemorrhage, ICCE appears to carry a relatively higher risk than ECCE with IOL. This is not the cases if only the progression of maculopathy is considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1996

Ultrastructure of surgically excised subfoveal neovascular membranes.

We studied the ultrastructural features of four consecutive subfoveal neovascular membranes (SFNM) associated with age-related macular degeneration. Cellular components of the membranes included retinal pigment epithelial (RPE) cells, endothelium-lined vascular channels, macrophages, myofibroblasts, fibrocytes, glial cells, erythrocytes, and lymphocytes. Extracellular interstitial constituents included collagen fibrils, basal laminar deposits, fibrin and young elastic fibrils. These findings show that SFNMs consist of various cells originating from surrounding tissues and vessels. Among these RPE cells and macrophages are the main cellular components and in conjunction with various extracellular matrix, especially collagen, may play an important role in the formation and maintenance of the membranes.

Basement Membrane↗
PubMed2006

Overexpression of FasL in retinal pigment epithelial cells reduces choroidal neovascularization.

Choroidal neovascularization (CNV) is responsible for the severe visual loss in age-related macular degeneration. CNV formation is considered to be due to an imbalance between pro- and antiangiogenic factors that lead to neovascular growth from the choriocapillaris into the subretinal space. To define whether FasL overexpression in retinal pigment epithelial cells (RPE) can inhibit choroidal neovascularization through Fas-FasL-mediated apoptosis, we examined the role of this pathway in a mouse model of laser-induced choroidal neovascularization. FasL was expressed in the retinal pigment epithelium of transgenic mice. Polymerase chain reaction (PCR), immunoblot, and immunohistochemistry confirmed that the transgene FasL was specifically expressed in RPE. The established laser model was used to induce choroidal neovascularization (CNV) in wild-type (WT) and transgenic mice. CNV formation was compared with respect to fluorescein angiographic leakage (at days 0 and 14 after laser injury) and histological appearance. The lesions were assessed on RPE-choroidal flatmounts after CD31-labeling and with confocal microscopy after perfusion with rhodamine-labeled concanavalin A (Con A). Apoptosis was quantified by TUNEL positivity and caspase activation. FasL mRNA and protein were highly expressed in the RPE of the transgenic mice before and after laser photocoagulation. In contrast, FasL was only weakly expressed in the RPE layer of WT C57BL/6J mice. While ruptures of Bruch's membrane and CNV formation were observed histologically two weeks after laser photocoagulation in transgenic as well as control eyes, the shape and size of CNV lesions were reduced in the transgenic mice. The area of leakage was decreased by 70% in FasL transgenic mice compared with WT mice (P<0.005). The number of TUNEL-positive cells was greater in FasL-overexpressing mice and correlated with the expression of activated caspases. Th expression of other antiangiogenic factors such as PEDF remained unchanged. The specific overexpression of FasL in RPE layer reduced CNV formation in our laser model. Our results strongly point to the FasL-Fas pathway as a potential therapeutic target in controlling pathological choroidal neovascularization.

Animals↗
PubMed2005

The Age-Related Eye Disease Study severity scale for age-related macular degeneration: AREDS Report No. 17.

OBJECTIVE: To develop a fundus photographic severity scale for age-related macular degeneration (AMD). METHODS: In the Age-Related Eye Disease Study, stereoscopic color fundus photographs were taken at baseline, at the 2-year follow-up visit, and annually thereafter. Photographs were graded for drusen characteristics (size, type, area), pigmentary abnormalities (increased pigment, depigmentation, geographic atrophy), and presence of abnormalities characteristic of neovascular AMD (retinal pigment epithelial detachment, serous or hemorrhagic sensory retinal detachment, subretinal or sub-retinal pigment epithelial hemorrhage, subretinal fibrous tissue). Advanced AMD was defined as presence of 1 or more neovascular AMD abnormalities, photocoagulation for AMD, or geographic atrophy involving the center of the macula. We explored associations among right eyes of 3212 participants between severity of drusen characteristics and pigmentary abnormalities at baseline and development of advanced AMD within 5 years of follow-up. RESULTS: A 9-step severity scale that combines a 6-step drusen area scale with a 5-step pigmentary abnormality scale was developed, on which the 5-year risk of advanced AMD increased progressively from less than 1% in step 1 to about 50% in step 9. Among the 334 eyes that had at least a 3-step progression on the scale between the baseline and 5-year visits, almost half showed stepwise progression through intervening severity levels at intervening visits. Replicate gradings showed agreement within 1 step on the scale in 87% of eyes. CONCLUSIONS: The scale provides convenient risk categories and has acceptable reproducibility. Progression along it may prove to be useful as a surrogate for progression to advanced AMD.

Atrophy↗
PubMed1993

[Changes of the diabetic retinopathy score].

Changes of the retinopathy score with the progression of diabetic retinopathy were investigated in 87 eyes of 44 diabetic patients. The previously reported retinopathy scoring system of Yamashita et al., utilizing fluorescein angiography, was used. Factors relevant to an increase of the retinopathy score were determined using quantification analysis (a type of multivariate analysis). The factors assessed were microaneurysms, the extent of retinal nonperfusion, intraretinal microvascular abnormalities, the grade of fluorescein dye leakage from retinal vessels, neovascularization, the grade of macular edema, the HbA1c level and the duration of retinopathy. The retinopathy score increased in 50 eyes (57%) after a mean follow-up period of 24.9 months. The probability of the score increasing in the eyes with advanced background retinopathy was 78%. The probability in eyes with preproliferative or proliferative diabetic retinopathy was 52% or 11%, respectively. The mean increase of the score in one year was 3.0 for all subjects. The increase in the eyes with advanced background, preproliferative or proliferative diabetic retinopathy was 6.1, 2.8 or 0.1, respectively. Our results suggest that this scoring system can effectively detect changes of background and preproliferative retinopathy. According to quantification analysis, the factor most relevant to the increase of the score was retinal nonperfusion. Dye leakage and neovascularization were also relevant, in descending order.

Diabetic Retinopathy↗
PubMed1989

The efficacy of panretinal photocoagulation for neovascularization of the iris after central retinal artery obstruction.

Panretinal photocoagulation (PRP) is widely used for a variety of ischemic ocular conditions. In diseases that produce neovascularization of the iris (NVI), such as diabetes mellitus and central retinal vein obstruction, a judiciously timed PRP can reduce the incidence of neovascular glaucoma. Neovascularization of the iris can occur after central retinal artery obstruction (CRAO) as well. In this article, the authors report the outcome of 17 patients who received PRP to treat rubeosis iridis secondary to CRAO. Eleven of the 17 patients (65%) showed regression of NVI after PRP. Although the uncontrolled and retrospective nature of this study precludes drawing definitive conclusions from these data, PRP appears to be effective in reducing the incidence of neovascular glaucoma, if it is delivered before the development of elevated intraocular pressure (IOP). Once neovascular glaucoma occurs, additional modalities appear to be necessary in order to adequately control the elevated IOP.

Aged↗