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Results for “Neovascularization, Pathologic”

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At least 1,027 records · Page 57Linked to original sources
PubMed1998

Do intraocular angiotensin II levels, plasma prothrombotic factors and endothelial dysfunction contribute to proliferative diabetic retinopathy?

PURPOSE: To investigate whether diabetic retinopathy (DR) is associated with abnormalities in: (i) aqueous humour Angiotensin I (Ang I) and Angiotensin II (Ang II) levels; and (ii) plasma Ang I, soluble P-selectin, lipoprotein (a) (Lp(a)), endothelial markers and haemorheological abnormalities. METHODS: Cross-sectional study of diabetic patients and healthy controls undergoing cataract surgery. RESULTS: 21 diabetic patients (12 males; mean age 67.0 years) were studied. Plasma levels of Ang II were lower in diabetics compared with controls (p<0.05). There were no differences in mean aqueous Ang I and Ang II levels in diabetics with or without proliferative DR compared with controls. Mean systolic blood pressure was higher in Group 1 patients (p=0.02). Patients with DR also demonstrated high Lp (a) and abnormal haemorheological factors (fibrinogen, white cell count). CONCLUSION: Ang I and Ang II do not significantly contribute to the pathogenesis of DR. Patients with DR also had abnormal Lp (a) and haemorheological factors. The role of hypertension in the pathogenesis of DR needs further evaluation.

Aged↗
PubMed2005

Gene transfer using the mature form of VEGF-D reduces neointimal thickening through nitric oxide-dependent mechanism.

Gene transfer to the vessel wall using vascular endothelial growth factors (VEGFs) has shown therapeutic potential for the treatment of restenosis. In this study, we evaluated the effect of catheter-mediated adenoviral (Ad) gene transfer of the mature form of VEGF-D (VEGF-D(DeltaNDeltaC)) in balloon-denuded cholesterol-fed rabbit aorta. AdLacZ was used as a control. Transduced VEGF-D(DeltaNDeltaC) mRNA was detectable in the arterial wall with RT-PCR at 6, 14 and 28 days. Gene transfer efficiency as detected with X-gal staining 6 days after the AdLacZ transduction was 1.91 +/- 1.32% in intima. AdVEGF-D(DeltaNDeltaC) gene transfer led to 52% reduction in intima/media ratio (I/M) as compared to the AdLacZ controls at 14 days time point. At 6 days there were no differences in I/M, but the number of macrophages in the vessel wall was 85% lower in the AdVEGF-D(DeltaNDeltaC) group as compared to the controls. The therapeutic effect was no longer detectable 28 days after the gene transfer. The therapeutic effect of VEGF-D(DeltaNDeltaC) was nitric oxide (NO)-dependent as the feeding of NO synthase inhibitor, L-NAME, blocked the reduction in intimal thickening. It is concluded that AdVEGF-D(DeltaNDeltaC) gene transfer reduces intimal thickening and macrophage influx into the vessel wall in balloon-denuded rabbit aortas.

Adenoviridae↗
PubMed2006

Nf1 haploinsufficiency augments angiogenesis.

Mutations in the NF1 tumor-suppressor gene underlie neurofibromatosis type 1 (NF1), in which patients are predisposed to certain tumors such as neurofibromas and may associate with vascular disorder. Plexiform neurofibromas are slow growing benign tumors that are highly vascular and can progress to malignancy. The development of neurofibromas requires loss of both Nf1 alleles in Schwann cells destined to become neoplastic and may be exacerbated by Nf1 heterozygosity in other non-neoplastic cells. This study tested the hypothesis that Nf1 heterozygosity exaggerates angiogenesis. We found that Nf1 heterozygous mice showed increased neovascularization in both the retina and cornea in response to hypoxia and bFGF, respectively, compared to their wild-type littermates. The increase in corneal neovascularization was associated with heightened endothelial cell proliferation and migration, and increased infiltration of inflammatory cells. In addition, Nf1 heterozygous endothelial cell cultures showed an exaggerated proliferative response to angiogenic factors, particularly to bFGF. These findings support the conclusion that Nf1 heterozygosity in endothelial cells and perhaps inflammatory cells augments angiogenesis, which may promote neurofibroma formation in NF1.

Animals↗
PubMed2000

The controls of microvascular survival.

The regulation of microvascular survival impacts both developmental remodeling of the vasculature, and various microvascular pathologies. In pathological settings of vascular insufficiency, molecular targets to affect stabilization of neovascularization are needed. Conversely, an important part of anti-tumor angiogenesis is the de-stabilization of the tumor vasculature. In the study of vascular remodeling, one difficult challenge is to understand the molecular controls that allow regression of one entire vessel segment and not another. This phenomenon requires coordination of the survival signaling pathways to successfully impact vascular structure. This review describes the known mechanisms and molecules involved in microvascular and endothelial cell survival. In particular the mechanisms of molecular signaling for survival in vitro are discussed in light of what is known about microvascular survival in vivo. Possible ways to bring these data together to explain the complex regulation of vessel survival are discussed.

Animals↗
PubMed2007

Combination angiostatic therapy completely inhibits ocular and tumor angiogenesis.

Angiostatic therapies designed to inhibit neovascularization associated with multiple pathological conditions have only been partially successful; complete inhibition has not been achieved. We demonstrate synergistic effects of combining angiostatic molecules that target distinct aspects of the angiogenic process, resulting in the complete inhibition of neovascular growth associated with development, ischemic retinopathy, and tumor growth, with little or no effect on normal, mature tissue vasculature. Tumor vascular obliteration using combination angiostatic therapy was associated with reduced tumor mass and increased survival in a rat 9L gliosarcoma model, whereas individual monotherapies were ineffective. Significant compensatory up-regulation of several proangiogenic factors was observed after treatment with a single angiostatic agent. In contrast, treatment with combination angiostatic therapy significantly reduced compensatory up-regulation. Therapies that combine angiostatic molecules targeting multiple, distinct aspects of the angiogenic process may represent a previously uncharacterized paradigm for the treatment of many devastating diseases with associated pathological neovascularization.

Angiogenesis Inhibitors↗
PubMed2001

Quantitation of the changes in vascularity during arthritis in the knee joint of a mouse with a digital image analysis system.

Many joint and bone diseases are caused by, or associated with vascular changes. Particularly in rheumatoid arthritis, vascular sprouting of synovial vessels plays a major role in the generation of joint pathology. To assess the effects of pharmaceuticals that are designed to inhibit neovascularization, we developed a quantitative procedure to measure vascular changes in cross-sections of the mouse knee joint during arthritic inflammation. Arthritis was induced in the knee joint of C57Black6 mice by a single subpatellar injection of methylated BSA after previous immunization. Total vascularity was visualized with a specific monoclonal rat anti-mouse antibody (9F1). Functional vessels were detected with the fluorescent perfusion marker Hoechst 33342. The localization of Hoechst and the vascular marker 9F1 were analyzed in separate images with an automated digital image processing system. By combining the two images, total vascularity and the perfusion status of the vessels during arthritis could be established. The digital image system measures synovial area (SA), number of all blood vessels (NBV) and the number of perfused blood vessels (NpBV). From these parameters the percentage of perfused vessels (perfusion fraction; PF), the vessel density (VD = NBV/SA) and the density of perfused vessels (VDp = NpBV/SA) can be calculated. The measurements showed that the area of synovial tissue had increased during arthritis. Moreover, both the number of blood vessels (NBV) and the number of perfused vessels (NpBV) in the synovial area had increased significantly on Days 4 and 7 after arthritis induction. This procedure enabled quantitation of total vascularity and of functional blood vessels in cross-sections of synovial tissue. It is expected to be a powerful tool, not only to analyze the effects of anti-angiogenic therapies in animal models of arthritis, but could also be applicable to study vascular and perfusion changes in vascular related diseases of the skeleton.

Animals↗
PubMed1995

Interferon gamma-inducible protein 10 (IP-10), a member of the C-X-C chemokine family, is an inhibitor of angiogenesis.

Angiogenesis is fundamental to a variety of physiological and pathological processes. While a number of factors have been identified that induce neovascularization, it is becoming increasingly apparent that endogenous angiostatic factors may play an important role in the regulation of angiogenesis during wound repair, chronic inflammation, and growth of solid tumors. In this study, we demonstrate the novel finding that IP-10, a member of the C-X-C chemokine family, is a potent inhibitor of both IL-8 and bFGF-induced angiogenic activity using in vitro and in vivo assays of angiogenesis. These findings support the contention that IP-10 may be a pivotal cytokine in the regulation of neovascularization.

Amino Acid Sequence↗
PubMed2001

Retinal ischemia and angle neovascularization in proliferative diabetic retinopathy.

PURPOSE: To analyze the relationship between the extent of retinal ischemia in proliferative diabetic retinopathy and angle neovascularization. METHODS: Panoramic fundus fluorescein angiography and 360-degree fluorescein gonioangiography to detect the angle neovascularization were performed on 70 eyes of 46 patients with proliferative diabetic retinopathy. Statistical significance was evaluated by chi-squared test. Statistical significance was evaluated if the value (T) was greater than the level of significance, chi(0.05)(2)(2) = 5.99. RESULTS: Retinal ischemia in fluorescein angiography was evaluated in four areas: capillary occlusion in (1) temporal raphe; (2) radial peripapillary capillaries; (3) the midperiphery (grade I, less than 25% of the area; grade II, 25% to 50%; grade III, 50% to 75%; grade IV, more than 75%); and (4) optic disk with neovascularization. The angle neovascularization was divided into two types: type I (14 eyes) and type II (12 eyes). Capillary occlusion in the temporal raphe and radial peripapillary capillaries, and papillary leakage significantly increased the risk of angle neovascularization (T = 8.28, 10.04, 6.44 respectively). Grade III and IV capillary occlusion in the midperiphery had a significant risk of angle neovascularization when compared with grade I (between grade III: T = 9.03, grade IV: T = 19.36) and II (between grade III: T = 6.31, grade IV: T = 16.09). CONCLUSION: Risk factors for angle neovascularization were retinal nonperfusion in the midperiphery wider than grade III, capillary occlusion in the radial peripapillary capillaries and temporal raphe, and optic disk. Fluorescein gonio angiography was found to be a powerful tool for the early detection of angle neovascularization, especially in dark irides.

Adult↗
PubMed2005

[Low-vision rehabilitation of age-related macular degeneration patients with retrofoveal choroidal new-vessels treated with photodynamic therapy with verteporfin].

PURPOSE: To demonstrate the rehabilitation benefit and immediate optical magnification and electronic equipment advantage in an age-related macular degeneration population with retrofoveal choroidal new-vessels treated by photodynamic therapy using Visudyne. PATIENTS AND METHODS: Sixty seven consecutive patients with retrofoveal choroidal new-vessels treated by Photodynamic Therapy using Visudyne were referred to an orthoptist for low-vision rehabilitation. The criteria investigated for this study were: long distance visual acuity, reading ability, contrast sensitivity, (before treatment and during post-treatment examinations), and fixation localization and optical equipment model. RESULTS: This study showed and studied visual acuity variations, mostly for patients with good visual acuity at inclusion. Contrast sensitivity stayed more or less the same. Retinal fixation was foveolar most of the time (68.7%). Optical or electronic devices for low-vision patients are numerous and video systems were the most currently used among our population. 62.7% des patients had low-vision rehabilitation with optic aids. DISCUSSION AND CONCLUSION: This study threw light on patient optic aids which must be prescribed according to his needs and difficulties, without delay. This equipment will then be readapted at each stage of the patient evolution. PDT treatment gives an important role to low-vision rehabilitation associated with optic magnification aids.

Aged↗
PubMed1982

The vascular response to contact lens wear.

The ocular limbal blood vessels were studied in daily wearers of soft contact lenses and hard contact lenses, and in eyes of subjects who had never worn a contact lens. The degree of filling of vessels and the number of vessels crossing the limbus were measured photographically at the inferior limbus. The extent to which vessel filling in contact lens wearers could be considered as capillary injection, as apposed to new vessel growth, was estimated by comparing the degree of injection in lens wearers to that found in nonwearers given a vasodilating stimulus. It was found that soft lens wearers showed greater limbal injection than hard lens wearers. The limbal vasculature of hard lens wearers was indistinguishable from that of nonwearers. The vascular response to soft lens wear was similar in magnitude to that produced by vasodilating agents in noncontact lens wearers, and was therefore considered to be due to the filling of preexisting capilliaries rather than new vessel growth. The chronic level of vessel dilation in soft lens wearers is cause for concern, as sustained dilation of the limbal vessels may be a precursor to new vessel growth.

Adult↗
PubMed2003

Sustained decrease in superoxide dismutase activity underlies constrictive remodeling after balloon injury in rabbits.

OBJECTIVE: The redox pathophysiology of vascular repair is incompletely understood. We assessed the role of vascular superoxide dismutase (SOD) activity in oxidative/nitrative stress and caliber loss postinjury (PI). METHODS AND RESULTS: Rabbits submitted to iliac artery balloon overdistension were followed for 14 days PI. Significant decrease in vascular SOD activity occurred at 7 and 14 days PI (by 45% and 34%, respectively, versus control, 96+/-1 U/mg, P<0.05). Separation in concanavalin-A column showed that both extracellular SOD (ecSOD) and CuZn SOD activities were reduced, whereas Western analysis showed normal or augmented protein expression. Immunoreactivity to nitrotyrosine, neuronal NO synthase (NOS), and inducible NOS (iNOS) increased in media and neointima PI; iNOS mRNA also augmented. Administration of ecSOD from days 7 to 14 PI corrected the SOD activity decrease and minimized caliber loss by 59% (P=0.007) despite unaltered neointima. Nitrate levels markedly increased with ecSOD in injured artery homogenates (26+/-5 versus 4+/-0.3 micromol/L per mg, P=0.001). Such increase was 70% inhibited by specific iNOS antagonist 1400w. Nitrotyrosine and neuronal NOS expression decreased after ecSOD. CONCLUSIONS: Sustained low vascular SOD activity has a key role in constrictive remodeling after injury, promoting oxidative/nitrative stress and impairment of iNOS-derived NO bioavailability. SOD function may critically determine whether iNOS induction is beneficial or deleterious in vivo.

Animals↗
PubMed2002

Angiogenesis in the central nervous system: a role for vascular endothelial growth factor/vascular permeability factor and tenascin-C. Common molecular effectors in cerebral neoplastic and non-neoplastic "angiogenic diseases".

Human pathological conditions of the central nervous system (CNS) associated with angiogenesis (i.e. neovascularization) include neoplastic, as well as infectious, ischemic, and traumatic processes. Upregulation of vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) and tenascin-C (TN-C) is spatially and temporally related to neovascularization. Spatially, VEGF/VPF and TN-C are both found at the site of neovascularization, but they are not detected in areas of normal brain or in areas without neovascularization. Temporally, VEGF/VPF and TN-C are found at the peak of angiogenesis and are not detected when angiogenesis had ceased.

Adult↗
PubMedDate not supplied

[Aging changes in conjunctival blood vessels].

The relation of the changes in the conjunctival blood vessels to the age were studied in a group of 217 persons aged 20 to 79 years. All persons suffering from arterial hypertension, diabetes, systemic diseases and manifested forms of arteriosclerosis were excluded. It has been proved that examination of the conjunctival blood vessels by means of the slot-lamp facilitates the study of the changes in the microscopic blood vessels in relation to the age. Most conspicuous was the increase of the meander course of the blood vessels, also the increasing number of blood vessels is more frequent in the group of older persons. Clusters of vessels and a narrowing of the diameter of the arterioles was seen only in persons over fifty years of age. The "upright" course of the arterioles was found only in individual cases and without any special dependence to age. Sacculations on the small veins and microaneurysms on the arterioles were not observed in any of the examined group of healthy persons.

Adult↗
PubMed1994

Indocyanine green video angiography in patients with age-related maculopathy-related retinal pigment epithelial detachments.

Previous studies have stressed the benefit of laser photocoagulation for patients with age-related macular degeneration (AMD) and well-defined subretinal neovascularization (SRN). However, such lesions account for only 30% of cases with exudative age-related maculopathy. Especially in patients with retinal pigment epithelial detachment (PED), SRN is usually occult. This study was performed to reveal the role of digital indocyanine green (ICG) video angiography in the diagnosis of SRN in patients with PED. A total of 34 patients with AMD-associated retinal PED participated in the current study and underwent fluorescein and ICG angiography using scanning laser ophthalmoscopy. In these patients fluorescein angiography revealed no distinct SRN, whereas in 21 eyes (62%) ICG angiography showed well-demarcated choroidal neovascularization. The present study demonstrates that SRN can be detected in more than 50% of patients with PED by means of ICG video angiography. Therefore, ICG video angiography improves the detection of SRN in patients with AMD-associated PED.

Aged↗
PubMed2001

An anti-angiogenic state in mice and humans with retinal photoreceptor cell degeneration.

Abnormal angiogenesis accompanies many pathological conditions including cancer, inflammation, and eye diseases. Proliferative retinopathy because of retinal neovascularization is a leading cause of blindness in developed countries. Another major cause of irreversible vision loss is retinitis pigmentosa, a group of diseases characterized by progressive photoreceptor cell degeneration. Interestingly, anecdotal evidence has long suggested that proliferative diabetic retinopathy is rarely associated clinically with retinitis pigmentosa. Here we show that neonatal mice with classic inherited retinal degeneration (Pdeb(rd1)/Pdeb(rd1)) fail to mount reactive retinal neovascularization in a mouse model of oxygen-induced proliferative retinopathy. We also present a comparable human paradigm: spontaneous regression of retinal neovascularization associated with long-standing diabetes mellitus occurs when retinitis pigmentosa becomes clinically evident. Both mouse and human data indicate that reactive retinal neovascularization either fails to develop or regresses when the number of photoreceptor cells is markedly reduced. Our findings support the hypothesis that a functional mechanism underlying this anti-angiogenic state is failure of the predicted up-regulation of vascular endothelial growth factor, although other growth factors may also be involved. Preventive and therapeutic strategies against both proliferative and degenerative retinopathies may emerge from this work.

Animals↗