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PubMed1987

Vitrectomy for progressive proliferative diabetic retinopathy.

We analyzed the results of 105 diabetic vitrectomy cases. The vitrectomies were performed for progressive fibrovascular proliferation that caused epiretinal membranes, vitreopapillary traction, florid neovascularization, or subhyaloid hemorrhage, with or without substantial preoperative visual loss. Eyes with inactive retinal neovascularization, dense vitreous hemorrhage, traction retinal detachment involving the macula, or combined traction and rhegmatogenous retinal detachment were excluded. Seventy-four eyes (70%) had improved final vision. The final vision was unchanged in eight eyes (8%) and was worse in 23 eyes (22%). Factors associated with a favorable visual prognosis included the following: age of 40 years or less, preoperative visual acuity of 5/200 or better, absence of preoperative iris neovascularization, preoperative panretinal photocoagulation, and absence of an iatrogenic retinal break.

Adult↗
PubMed1993

Dual-perspective analysis of vascular formations in sickle cell retinopathy.

OBJECTIVE: To examine the sickle cell retina in dual perspective (vascular patterns en bloc and structure in serial sections) to gain new insights into sickle cell retinopathy. METHODS: We analyzed the retinas of two patients with sickle cell disease (a 54-year-old patient with hemoglobin SC, heterozygous for the S and C mutation in the beta chain of the globin gene, and a 20-month-old patient with sickle cell anemia [SS], homozygous for the S mutation) using the previously described adenosine diphosphatase flat-embedding technique. RESULTS: The dual-perspective analysis afforded by our technique revealed that the primary site of occlusions was located at the precapillary level. An unusual neovascular formation, the hairpin loop, was observed in both patients' retinas and appeared to result from recanalization of the wall of an occluded vessel. Many autoinfarcted pre-retinal neovascular formations were observed in the older SC patient. Two patent preretinal formations were studied in detail and their evolution appeared to be influenced by mechanical factors. The vessels appeared to have been extruded from the retina, perhaps owing to hydrostatic pressure secondary to downstream occlusions. Small pigmented lesions consisting of retinal pigment epithelial cells ensheathing channels that resembled autoinfarcted vessels were found in the eye of the SC patient. CONCLUSIONS: This study illustrates unusual morphological features of intraretinal and preretinal neovascularization and of chorioretinal lesions in sickle cell retinopathy and suggests alternative mechanisms for their formation.

Adult↗
PubMed1982

Neovascular fundus abnormalities in peripheral uveitis.

Neovascular fundus abnormalities are an unusual complication of peripheral uveitis. Peripheral retinal neovascularization was seen in 11 patients, six of whom had retinal angioma-like lesions. Most of the patients had loss of vision caused by vitreous hemorrhage. In four additional patients with peripheral uveitis, neovascularization developed either at the disc or elsewhere in the posterior pole.

Adolescent↗
PubMed1997

Integrin chatter and vascular function in diabetic retinopathy.

The interplay between adhesion receptors and proteolytic cascades is crucial for cell proliferation and migration in the (patho-)physiology of vascular function. Disregulated angiogenesis in diabetic retinopathy appears to be associated with the appearance of advanced glycation end products that disturb interactions between capillary cells and extracellular matrix. Vitronectin receptor-type integrins are expressed on angiogenic endothelial cells and contribute to unwanted vascular sprouting in the retinal tissue. In a hypoxia-induced retinal neovascularization model, intervention with low molecular weight integrin antagonist resulted in significant reduction of unwanted angiogenesis indicating that this angiostatic therapy appears to be promising also for late complications in diabetes.

Diabetic Retinopathy↗
PubMed2006

Myeloid progenitors differentiate into microglia and promote vascular repair in a model of ischemic retinopathy.

Vision loss associated with ischemic diseases such as retinopathy of prematurity and diabetic retinopathy are often due to retinal neovascularization. While significant progress has been made in the development of compounds useful for the treatment of abnormal vascular permeability and proliferation, such therapies do not address the underlying hypoxia that stimulates the observed vascular growth. Using a model of oxygen-induced retinopathy, we demonstrate that a population of adult BM-derived myeloid progenitor cells migrated to avascular regions of the retina, differentiated into microglia, and facilitated normalization of the vasculature. Myeloid-specific hypoxia-inducible factor 1alpha (HIF-1alpha) expression was required for this function, and we also demonstrate that endogenous microglia participated in retinal vascularization. These findings suggest what we believe to be a novel therapeutic approach for the treatment of ischemic retinopathies that promotes vascular repair rather than destruction.

Animals↗
PubMed1994

Progressive proliferative diabetic retinopathy after transplantation of the pancreas. A case and a review of the topic.

The unusual case history of the development of a progressive diabetic retinopathy despite normal blood glucose after transplantation of the pancreas and despite panretinal laser coagulations is described. A 26-year-old male with diabetic background retinopathy underwent a segmental transplantation of the pancreas in 1988. One year after surgery, a progressive proliferative retinopathy despite normoglycemia was found, which required an intensive panretinal photocoagulation during the following months. However, despite massive retinal coagulations, vitreous hemorrhages and retinal neovascularizations continuously occurred, thus requiring two vitrectomies. After these procedures, visual acuity recovered distinctly. It is suggested that the 'point of no return' for the development of proliferative changes in the retina had been passed at a time when a background retinopathy was still present. The effect of normoglycemia during follow-up of patients with diabetic retinopathy, described in the literature, is compared to this unusual case history.

Adult↗
PubMedDate not supplied

Increased diode laser uptake in inner retinal layers after indocyanine green staining of the internal limiting membrane.

Intraoperative use of indocyanine green to stain the internal limiting membrane assists in its visualization and removal. This article describes increased uptake of diode laser energy by the superficial layers of the retina after indocyanine green staining of the internal limiting membrane in a patient with diabetic macular edema and a taut, attached posterior hyaloid. The patient was undergoing pars plana vitrectomy, removal of the posterior hyaloid, and indocyanine green-assisted peeling of the internal limiting membrane. In addition, panretinal diode laser endophotocoagulation was performed after discovering retinal neovascularization. In areas that were more intensely stained with indocyanine green, the clinical appearance and optical coherence tomography scans demonstrated markedly increased laser energy uptake in the superficial layers of the retina. This case indicates near-infrared or infrared laser procedures performed in areas of indocyanine green-stained internal limiting membrane may necessitate adjustment of laser power and technique.

Aged↗
PubMed2005

SDF-1 is both necessary and sufficient to promote proliferative retinopathy.

Diabetic retinopathy is the leading cause of blindness in working-age adults. It is caused by oxygen starvation in the retina inducing aberrant formation of blood vessels that destroy retinal architecture. In humans, vitreal stromal cell-derived factor-1 (SDF-1) concentration increases as proliferative diabetic retinopathy progresses. Treatment of patients with triamcinolone decreases SDF-1 levels in the vitreous, with marked disease improvement. SDF-1 induces human retinal endothelial cells to increase expression of VCAM-1, a receptor for very late antigen-4 found on many hematopoietic progenitors, and reduce tight cellular junctions by reducing occludin expression. Both changes would serve to recruit hematopoietic and endothelial progenitor cells along an SDF-1 gradient. We have shown, using a murine model of proliferative adult retinopathy, that the majority of new vessels formed in response to oxygen starvation originate from hematopoietic stem cell-derived endothelial progenitor cells. We now show that the levels of SDF-1 found in patients with proliferative retinopathy induce retinopathy in our murine model. Intravitreal injection of blocking antibodies to SDF-1 prevented retinal neovascularization in our murine model, even in the presence of exogenous VEGF. Together, these data demonstrate that SDF-1 plays a major role in proliferative retinopathy and may be an ideal target for the prevention of proliferative retinopathy.

Adrenal Cortex Hormones↗
PubMed1975

Choroido-vitreal neovascularization after argon laser photocoagulation.

Argon laser photocoagulation performed to destroy retinal neovascularization in two patients with proliferative sickle retinopathy and one patient with sarcoidosis was complicated by the development of choroidal neovascular tissue that extended through the photocoagulated retina into the vitreous. Attempts to obliterate the neovascular growth were successful in two cases. In the case that did not respond to repeated therapeutic procedures, the possibility of a direct communication with the long posterior ciliary artery was suggested by the presence of a chorioretinal defect in the vicinity of the photocoagulated area.

Adult↗
PubMed2005

Pharmacological and pharmacokinetic study of olmesartan medoxomil in animal diabetic retinopathy models.

A close relationship between the renin-angiotensin system and the pathophysiology of diabetic retinopathy has been suggested, several angiotensin II type 1 receptor (angiotensin AT1 receptor) antagonists being effective in animal models. Therefore, we examined the efficacy of an angiotensin AT1 receptor antagonist, olmesartan medoxomil (CS-866), in animal retinopathy models. In diabetic stroke-prone spontaneously hypertensive (SHRSP) rats, 4-week treatment with CS-866 prevented the elongation of oscillatory potential peaks dose-dependently which almost normalized at 3 mg/kg/day. Next, in oxygen-induced retinopathy mice, CS-866 at 1 mg/kg significantly prevented the retinal neovascularization. In these animal models, plasma concentrations of CS-866 were comparable to the in vitro IC50 value of the angiotensin AT1 receptor. In summary, our data demonstrated that CS-866 was effective in early and late stage retinopathy models through the inhibition of the angiotensin AT1 receptor. These findings suggest the possibility of CS-866 as a therapeutic agent for diabetic retinopathy.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2006

Involvement of circulating endothelial progenitor cells and vasculogenic factors in the pathogenesis of diabetic retinopathy.

PURPOSE: Retinal neovascularization in diabetes has been thought to follow the release of local angiogenic factors in the retina. We hypothesize that neovascularization of diabetic retinopathy is a systemic vasculogenesis rather than a local angiogenesis. Thus, we evaluate the concentrations of circulating endothelial progenitor cells (EPCs) and stem cell modulation factors such as vascular endothelial growth factor (VEGF), erythropoietin (Epo), and substance p (SP) in the peripheral blood of diabetic retinopathy patients. METHODS: We studied 15 normal controls and 45 type II diabetic patients (no DR group (n=15), NPDR group (n=15), and PDR group (n=15)). We measured circulating CD34+mononuclear cells (CD34+MNCs), c-Kit+mononuclear cells (c-Kit+MNCs) by flow cytometry. VEGF, Epo, and SP in the peripheral blood were measured by ELISA. RESULTS: The circulating CD34+MNCs and c-Kit+MNCs increased in the NPDR and PDR groups compared with the control group (P<0.01). Serum level of VEGF increased in the NPDR and PDR groups compared with the control group (P<0.05). The level of Epo elevated exclusively in the no DR group compared with the other three groups (P<0.01). Circulating SP level increased in the NPDR and PDR groups compared with the control group (P<0.05). SP and CD34+MNCs were shown to have increased correlation according to the diabetic retinopathy in the NPDR and PDR groups (r=0.440, P<0.05 and r=0.460, P<0.05, respectively). CONCLUSIONS: The present study is the first to demonstrate that CD34+MNCs, c-Kit+MNCs and their modulator are elevated in diabetic retinopathy patients. Therefore, it is possible that circulating EPCs and serum Epo, VEGF, and SP may be involved in the progression of diabetic retinopathy.

Aged↗
PubMed2001

Regulation of retinal capillary cells by basic fibroblast growth factor, vascular endothelial growth factor, and hypoxia.

Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) feature prominently in retinal neovascular diseases. Although the role of VEGF in retinal angiogenesis is well established, the importance of bFGF in this process requires further clarification. This study was undertaken to investigate the responses of retinal capillary cells (endothelial cells and pericytes) to bFGF under hypoxic conditions, as well as the potentially synergistic effects of bFGF and VEGF on the proliferation and cord formation of retinal endothelial cells. Cell proliferation was determined by cell number and by 3H-thymidine incorporation. Cord formation was assessed in three-dimensional gels of collagen type I. VEGF and bFGF increased 3H-thymidine incorporation by both cell types, an effect that was more pronounced in a hypoxic environment. Moreover, the proliferation of pericytes was stimulated to a greater extent by bFGF relative to VEGF. Endothelial migration in collagen gels, however, was induced more effectively by VEGF than by bFGF. A synergistic effect of VEGF and bFGF on cell invasion was observed in the collagen gel assay. VEGF and bFGF each augment proliferation of these cells, especially under hypoxia. We thus propose that these two cytokines have a synergistic effect at several stages of angiogenesis in the retina.

Animals↗
PubMed1997

The relationship between accumulation of advanced glycation end products and expression of vascular endothelial growth factor in human diabetic retinas.

Both advanced glycation end products and vascular endothelial growth factor are believed to play a role in the pathogenesis of diabetic retinopathy. It is known that vascular endothelial growth factor causes retinal neovascularization and a breakdown of the blood-retinal barrier; how advanced glycation end products affect the retina, however, remains largely unclear. The substance-Ne-(carboxymethyl)lysine is a major immunologic epitope, i.e. a dominant advanced glycation end products antigen. We generated an anti-Ne-(carboxymethyl)lysine antibody to investigate the relationship between the localization of advanced glycation end products and that of vascular endothelial growth factor in 27 human diabetic retinas by immunohistochemistry. Nine control retinas were also examined. In all 27 diabetic retinas, Ne-(carboxymethyl)lysine was located in the thickened vascular wall. In 19 of the 27 retinas, strand-shaped Ne-(carboxymethyl)lysine immunoreactivity was also observed around the vessels. In all 27 diabetic retinas, vascular endothelial growth factor revealed a distribution pattern similar to that of Ne-(carboxymethyl)lysine. Vascular endothelial growth factor was also located in the vascular wall and in the perivascular area. Neither Ne-(carboxymethyl)lysine nor vascular endothelial growth factor immunoreactivity was detected in the 9 control retinas. Vessels with positive immunoreactivity for Ne-(carboxymethyl)lysine and/or vascular endothelial growth factor were counted. A general association was noted between accumulation of Ne-(carboxymethyl)lysine and expression of vascular endothelial growth factor in the eyes with non-proliferative diabetic retinopathy (p < 0.01) and proliferative diabetic retinopathy (p < 0.05).

Aged↗
PubMed1980

Long-term anatomic and functional results of vitrectomy for diabetic retinopathy.

A long-term follow-up study of 130 eyes that had had initially successful vitrectomies for complications of proliferative diabetic retinopathy showed that only ten (8%) eyes had significant worsening of visual acuity at final examination (18 to 68 months after surgery), compared to the best visual acuity recorded during the first six months after surgery. Active flat retinal neovascularization was present at final examination in only three eyes (2%), and in no case did elevated fibrovascular proliferation occur. The type and incidence of important complications during the early and later postoperative periods indicated a low rate of late complications.

Adult↗
PubMed2004

Altered insulin signaling in retinal tissue in diabetic states.

Both type 1 and type 2 diabetes can lead to altered retinal microvascular function and diabetic retinopathy. Insulin signaling may also play a role in this process, and mice lacking insulin receptors in endothelial cells are protected from retinal neovascularization. To define the role of diabetes in retinal function, we compared insulin signaling in the retinal vasculature of mouse models of type 1 (streptozotocin) and type 2 diabetes (ob/ob). In streptozotocin mice, in both retina and liver, insulin receptor (IR) and insulin receptor substrate (IRS)-2 protein and tyrosine phosphorylation were increased by insulin, while IRS-1 protein and its phosphorylation were maintained. By contrast, in ob/ob mice, there was marked down-regulation of IR, IRS-1, and IRS-2 protein and phosphorylation in liver; these were maintained or increased in retina. In both mice, Phosphatidylinositol 3,4,5-trisphosphate generation by acute insulin stimulation was enhanced in retinal endothelial cells. On the other hand, protein levels and phosphorylation of PDK1 and Akt were decreased in retina of both mice. Interestingly, phosphorylation of p38 mitogen-activated protein kinase and ERK1 were responsive to insulin in retina of both mice but were unresponsive in liver. HIF-1alpha and vascular endothelial growth factor were increased and endothelial nitric-oxide synthase was decreased in retina. These observations indicate that, in both insulin-resistant and insulin-deficient diabetic states, there are alterations in insulin signaling, such as impaired PDK/Akt responses and enhanced mitogen-activated protein kinases responses that could contribute to the retinopathy. Furthermore, insulin signaling in retinal endothelial cells is differentially altered in diabetes and is also differentially regulated from insulin signaling in classical target tissues such as liver.

Animals↗
PubMed1984

Current concepts of the effect of oxygen on the developing retina.

The role of oxygen in the development of retrolental fibroplasia and the mechanism of oxygen changes in the developing retina are discussed. The primary effect of oxygen is one of Vascular closure and the secondary response, which occurs after removal from increased oxygen, is retinal neovascularization. A brief discussion of recent observations on the potential role of vitamin E in the prevention of retrolental fibroplasia is presented.

Animals↗
PubMedDate not supplied

[Laser treatment in diabetic retinopathy].

1050 eyes with diabetic retinopathy (670 preproliferatives retinopathies, 380 proliferatives retinopathies), was treated by laser argon photocoagulation. The laser photocoagulation is the election therapeutical method for the zones of neovascular perfusion, after angiofluorographic diagnosis. It is necessary to know very well the therapeutical indications and the correct technique adopted to each type of lesions. Also is necessary to obtain an equilibrium of the diabetic, especially in limitation of high variation of glycemia. In this study 20% of treated cases, was repeated the photocoagulation, and 10% of cases presented complications: vitreous hemorrhages, neovascular glaucoma, retinal detachment.

Diabetic Retinopathy↗
PubMed1998

Transforming growth factor-beta1 induces apoptotic cell death in cultured retinal endothelial cells but not pericytes: association with decreased expression of p21waf1/cip1.

Transforming growth factor-beta1 (TGF-beta1) regulates a variety of cellular functions. In several types of cells, for example, it acts as a growth inhibitor and an inducer of apoptotic cell death. Although one of the important modulators in retinal vascular development and retinal neovascularization, the effects of TGF-beta1 on retinal microvascular cells are not fully defined. We have found that proliferation of both bovine retinal endothelial cells (EC) and pericytes was inhibited by TGF-beta1 in a concentration-dependent manner. However, only retinal EC lost viability after exposure to increasing concentrations of TGF-beta1 (up to 10 microg/ml) in the presence of 2% fetal bovine serum. Dying EC exhibited the morphological and biochemical characteristics of apoptosis. Fragmented nuclei and chromatin condensation were apparent after staining with the fluorochrome Hoechst 33258 and the reagent ApopTag; moreover, gel electrophoresis of DNA from TGF-beta1-treated EC demonstrated degradation of chromatin into the discrete fragments typically associated with apoptosis. The addition of anti-TGF-beta1 neutralizing antibody abolished the apoptotic cell death induced by TGF-beta1. Because not all the EC in a given culture died after exposure to TGF-beta1, we separated the apoptosis-sensitive cells from those resistant to TGF-beta1 -mediated apoptosis and determined the expression of several proteins associated with this apoptotic pathway. Apoptosis of EC mediated by TGF-beta1 was associated with a decreased level of the cyclin-dependent kinase inhibitor p21waf1/cip1, compared with that observed in the apoptosis-resistant cells. In contrast, the translation product of the tumor-suppressor gene p53 was increased in the TGF-beta1-treated apoptotic cells. Thus, we propose that p21waf1/cip1 and p53 function in distinct pathways that are protective or permissive, respectively, for the apoptotic signals mediated by TGF-beta1.

Animals↗