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Results for “Neovascularization, Pathologic”

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At least 793 records · Page 44Linked to original sources
PubMed1996

[Value of indocyanine green angiography in localization of occult choroid neovascularization].

PURPOSE: To determine the role of Indocyanin Green (ICG) angiography in localizing occult new vessels associated with age-related macular degeneration (ARMD) and assess the possibilities of ICG guided laser photocoagulations. PATIENTS AND METHODS: Fluorescein and ICG angiographies (IMAGEnet system) of 62 patients with occult new vessels (ONV), serous (SPED) or vascular (VPED) pigment epithelium detachment have been studied. RESULTS: Based on fondoscopic examination and fluorescein angiography, 43 eyes (69%) disclosed ONV, 8 (13%) SPED and 11 (18%) VPED. Choroidal neovascularisation was confirmed by ICG angiography in 37 ONV cases (86%), in 8 (72%) VPED cases, but in no SPED. Conversion of ONV in classical neovascular membranes was possible in 19 ONV cases (44%) and in 6 (54%) VPED cases, making a laser photocoagulation possible in 9 eyes (36%). CONCLUSION: ICG angiography plays an important role in the evaluation, classification and laser treatment of patients with ONV secondary to ARMD.

Aged↗
PubMed1992

Atypical parafoveal telangiectasis with subsequent anterior and posterior segment neovascularization.

Bilateral parafoveal telangiectasis typically includes the presence of fluorescein staining of outer retinal capillaries, no macular ischemia, right-angled venules, and migration of pigment along these venules. In the bilateral form, atypical parafoveal telangiectasis with macular ischemia but without right-angled venules or migration of pigment along these venules has been reported in only five patients previously. An atypical case is presented of bilateral parafoveal telangiectasis complicated, not only by areas of macular nonperfusion, but also by peripheral ischemia with subsequent anterior and posterior segment neovascularization in the absence of any systemic abnormalities. As in previously reported cases, this patient had no evidence of right-angled venules or pigment migration. Pan-retinal photocoagulation resolved the rubeosis and caused regression of the retinal neovascularization.

Fluorescein Angiography↗
PubMed1991

Neovascularisation: has the angiogenic factor already been found?

Recently many soluble growth factors capable of influencing neovascularisation (angiogenesis) have been isolated and molecularly cloned. As such they are now available in a highly purified and active form. One or several of these already quite well known molecules may be of importance in the control of ocular neovascularisation. This article reviews what is presently known about growth factor control of neovascularisation with particular emphasis on both the eye and those factors that have already been molecularly cloned. In addition several recently reported inhibitors of neovascularisation are discussed. Such research is of particular interest to the ophthalmologist as knowledge gained in this area may allow for the use of both growth factors as well as growth factor inhibitors in the management of several ocular diseases involving neovascularisation.

Angiogenesis Inducing Agents↗
PubMed1990

Chorioretinal neovascular membranes complicating contusional eye injuries with indirect choroidal ruptures.

Chorioretinal neovascular membranes are a recognised but rare cause of late visual loss in eyes suffering contusional injuries. A series of eight cases is presented all with indirect choroidal ruptures involving the perifoveal region. Two main patterns of 'at risk' rupture were noted: a temporally situated rupture passing almost directly through the fovea, and a rupture which curves inferior or superior to the optic disc stopping just short of the fovea. In six of eight cases there was only a partial thickness rupture of the choroid. These neovascular membranes may present at any time after the original injury, either early (within six months of the injury), which could be related to persistence of the normal reparative neovascular response, or late (at least one year after the injury), which are more likely to have resulted from a secondary breakdown of the outer blood-retina barrier.

Adolescent↗
PubMedDate not supplied

Non-paralleled increase of hepatocyte growth factor and vascular endothelial growth factor in the eyes with angiogenic and nonangiogenic fibroproliferation.

Vascular endothelial growth factor (VEGF) has been known as principal angiogenic factor in vasculogenesis, tumor angiogenesis and ocular angiogenesis. Currently, hepatocyte growth factor (HGF) has been reported to play a major role in ocular angiogenesis. We studied distribution of both growth factors in angiogenic and non-angiogenic fibroproliferation to determine the correlation of VEGF and HGF in retinal angiogenesis. Concentrations of VEGF and HGF molecules in vitreous samples from 27 eyes with angiogenic proliferative diabetic retinopathy (PDR) and 9 eyes with non-angiogenic proliferative vitreoretinopathy (PVR) were measured by enzyme-linked immunosorbent assay (ELISA). Vitreous samples with idiopathic macular role (IMH) served as a control. Concentrations of VEGF in the angiogenic PDR were 4.3 +/- 5.8 ng/ml (mean +/- SD), and were significantly higher than in non-angiogenic PVR (0.5 +/- 0.1 ng/ml). No significant differences were observed on VEGF concentrations between PVR to control. On the contrary, HGF concentrations were significantly higher in PVR (22.5 +/- 21.8 ng/ml) than in control (6.9 +/- 5.2 ng/ml), those of PDR (24.0 +/- 16.3 ng/ml) were also significantly higher than control. Among PDR samples, VEGF concentration was significantly higher than in the subgroup with higher angiogenic activity represented by iris neovascularization, although there were no significant differences on HGF concentration between the subgroups. Focal increases in HGF on fibroproliferation in the eye regardless of the involvement of angiogenesis were not in remarkable relation with angiogenic activity, unlike VEGF. These data suggested a more extensive role of HGF than VEGF strictly related to angiogenesis.

Diabetic Retinopathy↗
PubMed2000

VEGF receptor signaling in tumor angiogenesis.

The growth of human tumors and development of metastases depend on the de novo formation of blood vessels. The formation of new blood vessels is tightly regulated by specific growth factors that target receptor tyrosine kinases (RTKs). Vascular endothelial growth factor (VEGF) and the Flk-1/KDR RTK have been implicated as the key endothelial cell-specific factor signaling pathway required for pathological angiogenesis, including tumor neovascularization. Inhibition of the VEGF tyrosine kinase signaling pathway blocks new blood vessel formation in growing tumors, leading to stasis or regression of tumor growth. Advances in understanding the biology of angiogenesis have led to the development of several therapeutic modalities for the inhibition of the VEGF tyrosine kinase signaling pathway. A number of these modalities are under investigation in clinical studies to evaluate their potential to treat human cancers.

Angiogenesis Inhibitors↗
PubMed2003

Technology evaluation: pegaptanib, Eyetech/Pfizer.

Eyetech Pharmaceuticals and Pfizer are co-developing the anti-vascular endothelial growth factor aptamer, pegaptanib, as an angiogenesis inhibitor for the potential treatment of age-related macular degeneration and diabetic macular edema, in addition to other ocular diseases. Gilead was previously investigating the aptamer for the potential treatment of cancer, however, no data have been published for this indication since 1999.

Angiogenesis Inhibitors↗
PubMed2006

Low level arsenic promotes progressive inflammatory angiogenesis and liver blood vessel remodeling in mice.

The vascular effects of arsenic in drinking water are global health concerns contributing to human disease worldwide. Arsenic targets the endothelial cells lining blood vessels, and endothelial cell activation or dysfunction may underlie the pathogenesis of both arsenic-induced vascular diseases and arsenic-enhanced tumorigenesis. The purpose of the current studies was to demonstrate that exposing mice to drinking water containing environmentally relevant levels of arsenic promoted endothelial cell dysfunction and pathologic vascular remodeling. Increased angiogenesis, neovascularization, and inflammatory cell infiltration were observed in Matrigel plugs implanted in C57BL/6 mice following 5-week exposures to 5-500 ppb arsenic [Soucy, N.V., Mayka, D., Klei, L.R., Nemec, A.A., Bauer, J.A., Barchowsky, A., 2005. Neovascularization and angiogenic gene expression following chronic arsenic exposure in mice. Cardiovasc.Toxicol 5, 29-42]. Therefore, functional in vivo effects of arsenic on endothelial cell function and vessel remodeling in an endogenous vascular bed were investigated in the liver. Liver sinusoidal endothelial cells (LSEC) became progressively defenestrated and underwent capillarization to decrease vessel porosity following exposure to 250 ppb arsenic for 2 weeks. Sinusoidal expression of PECAM-1 and laminin-1 proteins, a hallmark of capillarization, was also increased by 2 weeks of exposure. LSEC caveolin-1 protein and caveolae expression were induced after 2 weeks of exposure indicating a compensatory change. Likewise, CD45/CD68-positive inflammatory cells did not accumulate in the livers until after LSEC porosity was decreased, indicating that inflammation is a consequence and not a cause of the arsenic-induced LSEC phenotype. The data demonstrate that the liver vasculature is an early target of pathogenic arsenic effects and that the mouse liver vasculature is a sensitive model for investigating vascular health effects of arsenic.

Animals↗
PubMed2007

Role of nonproteolytically activated prorenin in pathologic, but not physiologic, retinal neovascularization.

PURPOSE: Recently, it was revealed that the inhibition of nonproteolytic activation of prorenin led to significant suppression of ocular inflammation in endotoxin-induced uveitis. The purpose of the present study was to investigate whether nonproteolytically activated prorenin plays a role in ischemia-induced retinal neovascularization. METHODS: C57BL/6 neonatal mice were reared in an 80% concentration of oxygen from postnatal (P) day 7 to P12, followed by room-air breathing to P17 to induce ischemia-initiated retinal neovascularization. Tissue localization of activated prorenin and prorenin receptor was examined by immunohistochemistry. Animals received intraperitoneal injections of handle-region peptide (HRP), a decoy peptide corresponding to the handle region of prorenin, which inhibits prorenin receptor-mediated upregulation of the renin-angiotensin system (RAS). A concanavalin A lectin perfusion-labeling technique was used to evaluate the areas of physiologic and pathologic retinal new vessels and the number of leukocytes adhering to the vasculature. Retinal mRNA expression and protein levels of intercellular adhesion molecule (ICAM)-1, vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1, and VEGFR-2 were examined by RT-PCR and ELISA. RESULTS: Retinal vessels in ischemic retinopathy eyes were positive for activated prorenin and prorenin receptor. Pathologic, but not physiologic, retinal neovascularization was significantly attenuated in HRP-treated mice compared with vehicle- or control peptide-treated animals. The number of adherent leukocytes was also significantly reduced. Retinal mRNA expression and protein levels of ICAM-1, VEGF, VEGFR-1, and VEGFR-2 in ischemic retinopathy were also significantly suppressed by the application of HRP. CONCLUSIONS: The present findings suggest that nonproteolytic activation of prorenin selectively promotes pathologic, but not physiologic, retinal neovascularization through the inflammatory processes related to pathologic neovascularization.

Animals↗