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Results for “Retinal Neovascularization”

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At least 649 records · Page 36Linked to original sources
PubMed2003

Diabetic patients and retinal proliferation: an evaluation of the role of vascular endothelial growth factor (VEGF).

Vascular endothelial growth factor (VEGF) has been shown to play a major role in intraocular neovascularisation in ischaemic retinal diseases. The aim of this study was to evaluate the concentration of VEGF in vitreous, aqueous and epiretinal membranes of diabetic and non-diabetic patients, with other pathological conditions requiring surgical intervention. Higher VEGF concentration were found in samples from the eyes of diabetic patients versus other pathologies as well as in epiretinal membranes versus the other eye compartments in diabetic patients. However, high VEGF levels were also found in retinal detachment and proliferative vitreoretinopathy of non-diabetic patients. We concluded that VEGF is produced locally and plays a fundamental, but not specific, role in diabetic retinal neovascularisation and proliferation.

Aqueous Humor↗
PubMed1992

[Clinical and fluorescein angiography changes in patients with central retinal vein occlusion. A unicenter study of 125 patients].

Between January 1986 and December 1989 we prospectively studied 125 patients with central retinal vein occlusion (CRVO). Documented by fundus photography and fluorescein angiography clinical and angiographic findings were analysed. The age of the patients was between 22 and 89 years with a mean of 60 years. 74 (59%) were male and 51 (41%) female. 63 (50.4%) right and 62 (49.6%) left eyes were affected. Arterial hypertension was found in 34 (37.2%) and diabetes mellitus in 18 (14.4%) of the patients. Glaucoma was present in 14 (11.2%). 11 (8.8%) patients had bilateral CRVO. Preretinal neovascularisation was found in 5 (4%), vitreous hemorrhage in 6 (4.8%) and a retinal detachment in 2 (1.6%) patients. Iris neovascularisation at time of first presentation was found in 8 (6.4%) of all patients, related to the number of ischemic type of CRVO in 17.7%. Cystoid macular edema was found in 77 (61.6%), ischemic maculopathy in 24 (19.2%) patients, and a combination of cystoid and ischemic maculopathy in 11 (8.8%). Mean visual acuity was 20/100. A non ischemic type was present in 80 (64%) an ischemic in 45 (36%) of patients. Mean visual acuity in the non ischemic type was 20/60 and highly significant better (p < 0.0001) than in the ischemic type with a mean visual acuity of 20/400 (Mann-Whitney test). The density of intraretinal hemorrhages (p = 0.0005) and type of maculopathy (p < 0.0001) were highly significant related to the ischemia type (chi-square method).

Adult↗
PubMed1992

[Severe occlusive bilateral retinal vasculitis within the scope of seronegative systemic lupus erythematosus].

Retinal vascular manifestation is the most common form of ophthalmic involvement in patients with systemic lupus erythematosus (SLE). Most frequently these consist of cotton-wool spots with or without intraretinal hemorrhages. Although rare, a more severe retinal vaso-occlusive disease, termed retinal vasculitis, has been described. We report on a 37-year-old white female with a 13-year follow-up of chronic discoid lupus erythematosus, which suffered massive bilateral visual loss coincident with the systemic exacerbation of her disease (proteinuria, pneumonia, serositis, leucopenia). The diagnosis of SLE was established with reference to the revised ARA-criteria (American Rheumatism Association). Ophthalmoscopy and fluorescein angiography revealed the typical aspect of a SLE-associated vaso-occlusive retinopathy on both eyes with marked ischemia of the macula. Immediate maximal immuno-suppressive therapy, early performed panretinal photocoagulation and subsequent cryoretinopexy did not stop the progression of the disease. Six months after the initial event vascularisations of the disc and rubeosis iridis occurred, but no secondary glaucoma up to date. In this patient, the almost complete absence of characteristic autoantibodies and immunological markers was striking. The correlation with other lupus manifestations, different therapeutic concepts and prognostic factors in SLE-associated retinal vasculitis are discussed.

Adult↗
PubMed1991

[46-year follow up of malignant transformation of choroid nevus with vascularized surface drusen].

The unusual long and atypical clinical course of a prominent black choroidal tumor is presented. It was stationary for decades and became symptomatic for many years. The histologic findings post mortem showed a choroidal nervus with focal malignant change. Its symptoms were obviously caused by subretinal vascularized soft drusen. Only two histologic descriptions of this little-known change over choroidal nevi and two of histologically proven malignant transformations of choroidal nevi are published up to now.

Adult↗
PubMed1990

[Immunohistochemical differentiation of periretinal membranes].

The etiology of periretinal membranes, a complication of various ocular diseases, trauma, and ocular surgery, is still unknown. In the study reported here, 134 surgically removed periretinal membranes were semiquantitatively analyzed by immunohistochemical and morphological method (antigens S 100, GFAP, leukocyte antigens, factor 8; fibrosis). It was found that the cell population of the membranes varied both morphologically and immunohistochemically according to the disease. However, the RPE cell count did not correlate with the number of retinal tears recorded in the patients' histories.

Diabetic Retinopathy↗
PubMed1990

[Laser therapy of diabetic maculopathy. A comparative study of the argon green laser and dye red laser].

One hundred eyes with (pre)-proliferative diabetic retinopathy underwent central laser treatment for macular involvement. Fifty eyes were treated with the dye red 630 nm, the other 50 with the argon green 514 nm laser. Eighty of the eyes had previously undergone panretinal photocoagulation; in the other 20 this was performed 1.5-3 months after treating the macula because the central retinal changes were predominant. In accordance with the clinical angiographic classification of diabetic maculopathy, into an exudative, an edematous, and an ischemic type, three photocoagulation techniques were employed as appropriate, i.e., focal coagulation, (modified) grid coagulation, and extensive centripetal panretinal coagulation. Neither postoperative visual acuity, nor the fluorescein angiogram, nor fundus color photography revealed any significant difference in the results obtained with the two laser wavelengths.

Diabetic Retinopathy↗
PubMed2000

Vascular endothelial growth factor induces expression of connective tissue growth factor via KDR, Flt1, and phosphatidylinositol 3-kinase-akt-dependent pathways in retinal vascular cells.

Fibroblastic proliferation accompanies many angiogenesis-related retinal and systemic diseases. Since connective tissue growth factor (CTGF) is a potent mitogen for fibrosis, extracellular matrix production, and angiogenesis, we have studied the effects and mechanism by which vascular endothelial growth factor (VEGF) regulates CTGF gene expression in retinal capillary cells. In our study, VEGF increased CTGF mRNA levels in a time- and concentration-dependent manner in bovine retinal endothelial cells and pericytes, without the need of new protein synthesis and without altering mRNA stability. VEGF activated the tyrosine receptor phosphorylation of KDR and Flt1 and increased the binding of phosphatidylinositol 3-kinase (PI3-kinase) p85 subunit to KDR and Flt1, both of which could mediate CTGF gene induction. VEGF-induced CTGF expression was mediated primarily by PI3-kinase activation, whereas PKC and ERK pathways made only minimal contributions. Furthermore, overexpression of constitutive active Akt was sufficient to induce CTGF gene expression, and inhibition of Akt activation by overexpressing dominant negative mutant of Akt abolished the VEGF-induced CTGF expression. These data suggest that VEGF can increase CTGF gene expression in bovine retinal capillary cells via KDR or Flt receptors and the activation of PI3-kinase-Akt pathway independently of PKC or Ras-ERK pathway, possibly inducing the fibrosis observed in retinal neovascular diseases.

Animals↗
PubMed1999

Basement membrane and growth factor gene expression in normal and diabetic human retinas.

PURPOSE: Recently, we found abnormal accumulation of several extracellular matrix components in retinal basement membranes in human diabetic retinopathy (DR). Others have described increased levels of various growth factors within the vitreous of DR patients. This study examined mRNA levels of these extracellular matrix components and growth factors within human retinal tissues. METHODS: Total retinal RNA was analyzed by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR). RT-PCR products were identified by Southern blotting. Samples were normalized with respect to beta2-microglobulin cDNA. Twenty-one retinas were analyzed: 6 normal, 7 diabetic without DR and 8 diabetic with DR. RESULTS: In diabetic retinas without DR, the expression levels of most genes were similar to normal. In DR retinas, tenascin-C mRNA expression increased compared to both normal and diabetics without DR. By RT-PCR and Northern blotting, mainly small tenascin-C mRNA isoforms were expressed, and some of them were elevated in DR retinas. Fibronectin mRNA was elevated in DR compared to normal retinas, possibly due to the overexpression of extradomain A-containing isoform (ED-A+, or cellular fibronectin). In DR retinas, gene expression of vascular endothelial growth factor and placenta growth factor was elevated compared to normal, although mRNA for these growth factors receptors (VEGFR-1/Flt-1 and VEGFR-2/KDR) did not change significantly. Transforming growth factor-beta1 mRNA also increased in DR retinas. CONCLUSIONS: The data suggest that proliferative DR development may be associated with increased retinal expression of vascular endothelial growth factor, placenta growth factor and transforming growth factor-beta1 that possibly triggers the deposition of small tenascin-C isoforms in the blood vessel walls. Angiogenesis-stimulating tenascin-C may further promote diabetic retinal neovascularization.

Aged↗
PubMed2003

Three novel polymorphisms in the promoter region of the TIMP-3 gene are not associated with proliferative diabetic retinopathy in type 2 diabetes mellitus.

PURPOSE: Tissue inhibitor of metalloproteinase-3 (TIMP-3) is a member of the TIMP family of proteins, playing a significant role in the control of extracellular matrix remodelling. TIMP-3 might play a role in the regulation of retinal neovascularization during progression of diabetic retinopathy. Recently, three novel polymorphisms (-899T/A, -915A/G and -1296T/C) in the promoter region of the TIMP-3 gene have been identified. The aim of the study was to investigate a possible association of these polymorphisms with proliferative diabetic retinopathy (PDR) in type 2 diabetes mellitus (T2DM). METHODS: Genotypes were detected by polymerase chain reaction and subsequent restriction with specific endonucleases. Allele frequencies were determined in an association study comprising three groups of subjects (n = 371). RESULTS: Linkage disequilibrium was found among the three polymorphisms (P < or = 0.01). Allele frequencies did not differ between neither T2DM + PDR and T2DM non-PDR subjects (P > 0.05) nor between all T2DM versus non-diabetic subjects (P > 0.05). CONCLUSIONS: Polymorphisms in the promoter region of the TIMP-3 gene were not associated with the PDR in the Caucasian T2DM patients.

Diabetes Mellitus, Type 2↗
PubMed2003

Ibuprofen improves oxygen-induced retinopathy in a mouse model.

PURPOSE: Retinopathy of prematurity is a developmental vascular anomaly occurring in the incompletely vascularized retina of the premature infant. Ibuprofen is a nonsteroidal anti-inflammatory agent similar to indomethacin, but with less pronounced side-effects. The goal of the study was to test the hypothesis that ibuprofen would improve oxygen-induced retinopathy in a mouse model. METHODS: C57BL6 mice pups were exposed to 75% oxygen from postnatal day 7 through postnatal day 12. Ibuprofen was administered along with oxygen exposure as a single subcutaneous dose of 40 mg/kg/day for 5 days. Animals were sacrificed on postnatal day 17 through postnatal day 20. The severity of retinopathy was assessed by a retinopathy scoring system of fluorescein-conjugated dextran-perfused retinal flat mounts and by quantitation of extra-retinal nuclei by use of periodic acid-Schiff-stained retinal sections. RESULTS: Animals that received ibuprofen during hyperoxia exposure had a significantly lower median (25th, 75th quartile) retinopathy score of 6 (5, 7.5) compared with animals that received oxygen only, with a score of 12 (10.5, 12.5), with p < 0.005. Animals given ibuprofen during hyperoxia exposure had a significantly lower extra-retinal nuclei count per section (14.2 +/- 3.6) compared with animals that were only exposed to oxygen (26.8 +/- 5.8), with p < 0.005. Ibuprofen did not affect the growth of the animals. CONCLUSION: Ibuprofen improves oxygen-induced retinopathy when administered concurrently with the injury phase without affecting the normal retinal development of the animals.

Animals↗
PubMed2000

Retinal vascular changes induced by the oxidative stress of alpha-tocopherol deficiency contrasted with diabetic microangiopathy.

It has been proposed that oxidative tissue damage is involved in the development of diabetic angiopathies. To evaluate this hypothesis, experiments were conducted to identify the retinal vessel changes induced by the oxidative stress related to alpha-tocopherol deficiency and examine possible similarities with the lesions characteristic of diabetic retinopathy. Twenty-one-day-old male Fisher 344 albino rats were divided randomly to receive a basal, chemically defined diet either with (adequate group) or without (deficient group) alpha-tocopherol. After 6 and 8 months, some rats (n = 3 per group) were killed and the eyes removed. In order to evaluate cell integrity and localization of lipofuscin-specific autofluorescence by light and fluorescence microscopy, some of the retinas were prepared for cryostat-sections while others were digested by elastase to isolate intact retinal vasculatures. After 8 and 14 months, the central retina of one eye per rat (n = 6 to 8 per group) was examined by electron microscopy for retinal capillary basement membrane (RCBM) thickening and other ultrastructural changes. At 6 and 8 months, the deficient rats exhibited extensive shortening and disarray of rod outer segments (ROS), marked loss of photoreceptor cells, and pronounced increases in the numbers of granules with lipofuscin-specific autofluorescence in the retinal pigment epithelium (RPE) and retinal vessels. At 14 months, the ultrastructure revealed that the damage to ROS involved disruption of membranes and that the capillary lipofuscin was contained mainly within the endothelial cells. Membrane remnants were found in the lipofuscin granules of both the RPE and retinal vessels. In addition, there was an increase in RCBM thickness (98.7 +/- 2.6 nm vs. 86.9 +/- 2.9 nm). RCBM thickening was the only finding common with diabetic retinopathy, and the thickening was 13.6%, significantly less than that reported in diabetic rat models with 8 and 14 months durations (34% and 53.1%, respectively). Capillary lipofuscin accumulation, which was prominent in the deficient rats, is not notable in diabetes. Both the moderate RCBM thickening and marked lipofuscin accumulations seen in alpha-tocopherol-deficient rats were similar to changes occurring in the aging process, though more pronounced. The spectrum of microangiopathies characteristic of diabetic retinopathy did not develop in alpha-tocopherol-deficient rats. These findings suggest that oxidative damage, though probably involved, is unlikely to play a predominant role in the development of diabetic retinal microangiopathies.

Animals↗
PubMed2006

Inhibitive effect of genistein on hypoxia-induced basic fibroblast growth factor expression in human retinal pigment epithelium cells.

AIM: The time course changes of basic fibroblast growth factor (bFGF) expression induced by hypoxia and the effects of genistein on hypoxia-induced bFGF expression in the human retinal pigment epithelium (RPE) cells were studied. METHODS: The bFGF mRNA expression was examined by reverse transcription polymerase chain reaction. The bFGF protein expression was detected by Western blot. RESULTS: Hypoxia significantly increased bFGF mRNA expression. The maximal level detected at 24 h was approximately two times that at the start of treatment. With pretreatment of genistein (10, 20, 50, 100, and 200 microM) for 30 min, the elevated expression of bFGF mRNA was suppressed in a concentration-dependent manner. bFGF mRNA expression was reduced to 30.4% by 200 microM of genistein when compared with that untreated with genistein. Hypoxia treatment also remarkably increased the expression of bFGF protein. At 24 h after hypoxia, when the highest expression of bFGF protein was observed, it was approximately two times as much as that at the start of treatment. Genistein (10, 20, 50, 100, and 200 microM) could also suppress bFGF protein expression in a concentration-dependent manner. The highest suppression was observed when exposed to 200 microM of genistein, which was 43% of control. CONCLUSIONS: These results suggested that suppression of bFGF expression in RPE cells might partly account for the inhibitive effect of genistein on retinal neovascularization in vivo.

Angiogenesis Inhibitors↗
PubMed1997

Subretinal hemorrhages in proliferative diabetic retinopathy.

PURPOSE: To describe the clinical features of patients with advanced proliferative diabetic retinopathy who underwent vitrectomy and were found to have subretinal hemorrhages. METHODS: The authors conducted a retrospective study of 49 patients with complications of proliferative diabetic retinopathy requiring pars plana vitrectomy and demonstrating the presence of subretinal hemorrhage. Preoperative, intraoperative, and postoperative clinical characteristics were evaluated. Patients were observed for a minimum of 6 months. RESULTS: The location, size, and clearance of subretinal hemorrhages revealed wide variation. Forty-two patients had focal subretinal hemorrhages, and 14 patients within this group had submacular hemorrhages. A retinal break was observed in 15 patients (31%). Only one patient required drainage of the subretinal hemorrhage to achieve retinal reattachment. Vitreous surgery resulted in 59% of patients achieving a visual acuity > or = 5/200. Seventy-nine percent had stable or improved vision, whereas 20% had worse vision after surgery. CONCLUSION: Subretinal hemorrhages appear to be an uncommon feature associated with long-term, advanced proliferative diabetic retinopathy and portend a guarded visual prognosis. These hemorrhages may occur spontaneously in previously untreated eyes and are often unsuspected until observed at the time of vitreous surgery. In general, removal of subretinal hemorrhages was not necessary to achieve macular anatomic attachment, and most patients experienced improved visual function after surgery. Diabetic subretinal hemorrhages may indicate a retinal break, and, therefore, careful ophthalmic inspection should be performed in these patients.

Adolescent↗