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PubMed2002

Pericytes and the pathogenesis of diabetic retinopathy.

Pericytes provide vascular stability and control endothelial proliferation. Pericyte loss, microaneurysms, and acellular capillaries are characteristic for the diabetic retina. Platelet-derived growth factor (PDGF)-B is involved in pericyte recruitment, and brain capillaries of mice with a genetic ablation of PDGF-B show pericyte loss and microaneurysms. We investigated the role of capillary coverage with pericytes in early diabetic retinopathy and the contribution to proliferative retinopathy using mice with a single functional allele of PDGF-B (PDGF-B(+/-) mice). As assessed by quantitative morphometry of retinal digest preparations, pericyte numbers in nondiabetic PDGF-B(+/-) mice were reduced by 30% compared with wild-type mice, together with a small but significant increase in acellular capillaries. Pericyte numbers were reduced by 40% in diabetic wild-type mice compared with nondiabetic wild-type controls. Pericyte numbers were decreased by 50% in diabetic PDGF-B(+/-) mice compared with nondiabetic wild-type littermates, and the incidence of acellular capillaries was increased 3.5-fold when compared with nondiabetic PDGF-B(+/-) mice. To investigate the effect of pericyte loss in the context of ongoing angiogenesis, we subjected mice to hypoxia-induced proliferative retinopathy. As a result, PDGF-B(+/-) mice developed twice as many new blood vessels as their wild-type littermates. We conclude that retinal capillary coverage with pericytes is crucial for the survival of endothelial cells, particularly under stress conditions such as diabetes. At high vascular endothelial growth factor levels, such as those in the retinopathy of prematurity model, pericyte deficiency leads to reduced inhibition of endothelial proliferation in vivo.

Animals↗
PubMed1994

Preventive eye care in people with diabetes is cost-saving to the federal government. Implications for health-care reform.

OBJECTIVE: Diabetic retinopathy, which leads to macular edema and retinal neovascularization, is the leading cause of blindness among working-age Americans. Previous research has demonstrated significant cost savings associated with detection of eye disease in Americans with type I diabetes. However, detection and treatment of eye disease among those with type II diabetes was previously thought not to be cost-saving. Our purpose was to estimate the current and potential federal savings resulting from the screening and treatment of retinopathy in patients with type II diabetes, based on recently available data concerning efficacy of treating both macular edema and neovascularization along with new data on federal budgetary costs of blindness. RESEARCH DESIGN AND METHODS: We used computer modeling, incorporating data from population-based epidemiological studies and multicenter clinical trials. Monte Carlo simulation was used, combined with sensitivity analysis and present value analysis of cost savings. RESULTS: Screening and treatment for eye disease in patients with type II diabetes generates annual savings of $247.9 million to the federal budget and 53,986 person-years of sight, even at current suboptimal (60%) levels of care. If all patients with type II diabetes receive recommended care, the predicted net savings (discounted at 5%) exceeds $472.1 million and 94,304 person-years of sight. Nearly all savings are associated with detection and treatment of diabetic macular edema. Enrolling each additional person with type II diabetes into currently recommended ophthalmological care results in an average net savings of $975/person, even if all costs of care are borne by the federal government. CONCLUSIONS: Our analysis indicates that prevention programs aimed at improving eye care for patients with diabetes not only reduce needless vision loss but also will provide a financial return on the investment of public funds.

Blindness↗
PubMed2002

Deficit of somatostatin-like immunoreactivity in the vitreous fluid of diabetic patients: possible role in the development of proliferative diabetic retinopathy.

OBJECTIVE: To evaluate the vitreous levels of somatostatin-like immunoreactivity (SLI) in patients with proliferative diabetic retinopathy (PDR). RESEARCH DESIGN AND METHODS: A total of 14 diabetic patients with PDR, in whom a vitrectomy was performed, were included in the study. Sixteen nondiabetic patients, with other conditions requiring vitrectomy, served as a control group. Both venous blood and vitreous samples were collected at the time of vitreoretinal surgery. Patients in whom intravitreous hemoglobin was detectable were excluded. In addition, a correction for plasma levels of SLI and intravitreal proteins was performed. SLI was measured by radioimmunoassay and vitreous hemoglobin by spectrophotometry. RESULTS: SLI in the vitreous fluid was significantly lower in diabetic patients than in the control group (68 +/- 18.7 vs. 193.6 +/- 30.8 pg/ml, P < 0.01). The vitreous SLI-to-plasma SLI ratio was strikingly higher in nondiabetic subjects than in diabetic patients with PDR (5.3 [1.2-71.1] vs. 0.6 [0.03-4.1], P < 0.01). After correcting for total vitreous protein concentration, SLI (pg/mg of proteins) remained significantly higher in nondiabetic control subjects than in diabetic patients with PDR (186 [51-463] vs. 7.5 [0.8-82], P < 0.0001). Remarkably, intravitreous levels of SLI were higher than those obtained in plasma in nondiabetic control subjects (193.6 +/- 30.8 vs. 43.5 +/- 10.7 pg/ml, P < 0.0001). Finally, a lack of relationship between plasma and vitreous levels of SLI was observed in both diabetic patients with PDR and nondiabetic control subjects. CONCLUSIONS: The significantly higher SLI in the vitreous fluid than in plasma detected in nondiabetic control subjects supports the concept that somatostatin plays a relevant role in retinal homeostasis. In addition, the intravitreous deficit of SLI observed in diabetic patients with PDR suggests that it might contribute to the process of retinal neovascularization.

Age of Onset↗
PubMed1986

Presence of endothelial cell growth factor activity in normal and diabetic eyes.

Two classes of growth factors affecting endothelial cell proliferation have been found previously in ocular tissues: a heat labile mitogen from retina (RDGF) and a heat stable inhibitor of proliferation from vitreous. The relative amounts of these growth factors in normal and diabetic cadaver eyes were investigated using fetal bovine aortic endothelial cell proliferation as an assay. Equivalent levels of RDGF activity were extracted from diabetic and normal sensory retinas. An extract from pigment epithelium and choroid was found to have similar levels of mitogenic activity, but this activity was not as heat labile as RDGF. Like RDGF, equivalent amounts of mitogen were extracted from diabetic and normal tissue. Normal human vitreous inhibited endothelial cell proliferation, and this activity was enhanced by heating the material (10 min., 95 degrees C). Four of the five individual diabetic vitreous samples of identical postmortem times were mitogenic when not heated, and exhibited little or no inhibitory activity when heated. Vitreous of identical postmortem times was pooled and fractionated by heparin-Sepharose chromatography to determine if the heat labile mitogen in vitreous was RDGF. From the insulin-dependent diabetic (IDDM) pooled vitreous sample, a prominent protein of 18 Kd was eluted from the column with 1.2 M NaC1, a characteristic of RDGF. This work suggests that both RDGF and the vitreous inhibitor are found in human vitreous, but their relative concentrations may change in the diabetic state so that retinal neovascularization from retina can occur.

Animals↗
PubMed1993

Fluorescein angiography as a means of assessing retinal vascular pathology in oxygen-exposed newborn rats.

Recently a new technique was reported in which examination of the retina of oxygen reared newborn rats was made using indirect fluorescence microscopy (Invest. Ophthal. Vis. Sci. 31:810). We have now improved this technique and systematically employed it as a means of studying oxygen-induced retinopathy in the newborn rat as an animal model for retinopathy of prematurity (ROP). Immediately after birth, litters of pigmented rats were exposed to an elevated oxygen atmosphere that varied in a cyclic fashion between 40% and 80% every 12 hours for 14 days. Rats raised simultaneously in room air served as controls. At the end of the treatment period, rats were deeply anesthetized, their pupils dilated, and 100 microliters of 3% sodium fluorescein was administered via tail venipuncture. After angiography, rats were awakened and returned to their mothers in room air for future assessment. Angiography was performed again at 4, 7, 38 or 56 days after oxygen treatment. Our results suggest that retinal pathology in the rat model parallels that of the human infant with ROP with respect to loss of patent retinal blood vessels in oxygen and subsequent abnormal vasoproliferation upon return to room air. Angiograms performed on room air-raised control rats at 14 days of age demonstrated our ability to resolve the smallest retinal capillaries. Angiograms conducted at the same age in oxygen-exposed rats revealed extensive areas of retinal non-perfusion and substantial arterio-venous shunting between adjacent primary vessels. If rats were maintained in room air for 4 or 7 days following oxygen exposure, a variety of pathologic signs became obvious including: 1) tortuosity of primary vessels mimicking human "plus disease", 2) frequent abnormal budding of tertiary vessels and capillaries, 3) retinal fluorescein leaks indicative of hemorrhages and 4) abnormal capillary tufts not evident at the time of removal from oxygen. By 38 and 56 days post-exposure, all four of these phenomena were still observed. Many of these pathologic phenomena could not have been observed with conventional methods currently used for retinal vascular assessment in small animals.

Animals↗
PubMed1993

The fractal geometry of proliferative diabetic retinopathy: implications for the diagnosis and the process of retinal vasculogenesis.

10 retinal vessel patterns with neovascularisation at or near the optic disk (NVD) from eyes of patients with diabetic retinopathy were compared with vascular patterns from 14 normal eyes. The vascular patterns were taken from low angle fundus photographs. After digitizing, the fractal dimensions were calculated by means of the density-density correlation function method. The fractal dimension was found to be significantly higher for vessel patterns with NVD [D = 1.845 +/- 0.056 (m +/- sd)] as compared with the normal control group (D = 1.708 +/- 0.073) (p < 0.001). The fractal dimension of 1.8 appears to be a cutoff value. Higher values may indicate proliferative changes. Under these conditions the sensitivity of the method for the detection of NVD > or = Grade 3 in the Early Treatment Diabetic Retinopathy Study (ETDRS) grading system is 90%. The presence of such NVD in an eye is a "high risk characteristic" for severe visual loss, which requires panretinal laser treatment. Fractal analysis is therefore a possible new strategy for computer assisted "automated" detection and quantification of proliferative diabetic retinopathy. The fractal dimension of the new vessels suggests possible mechanisms involved in retinal vasculogenesis.

Diabetic Retinopathy↗
PubMed1995

Mechanisms in retinal vasculogenesis: an analysis of the spatial branching site correlation.

Starting from fractal dimension calculations of retinal vessel patterns, different growth models and related mechanisms have been suggested to simulate retinal vasculogenesis. A comprehensive view of this topic does not exist. In order to elucidate this question the spatial correlation of the vessel branching sites of the embryonic vessel pattern has been studied. During development of the retinal vasculature within the nerve fiber layer a modification of the branching characteristics can be observed. This result supports theories which suggest a close relation between the vessel propagation and the structure and surface characteristics of the invading vascular cells and the retinal tissue. Arterio-venous differentiation, however, may be dominated by diffusion processes.

Animals↗
PubMedDate not supplied

Regression pattern in retinopathy of prematurity.

We characterized the regression pattern of retinopathy of prematurity (ROP) for 266 infants examined over a 22-month period. Infants were included in the evaluation with a birth weight of less than or equal to 1500 g. Regression of retinopathy was observed in all but 11 infants, who were treated for threshold ROP. ROP limited to the peripheral retina resolved around term (40 weeks postconceptional age). Posterior ROP and/or stage 3 ROP underwent a protracted course of resolution, often not reaching zone 3 until 42 to 45 weeks after conception. Permanent retinal/vascular sequelae of ROP were observed in 10% of infants with ROP. The most common abnormality was failure to completely vascularize the temporal retinal periphery. Overall, retinal morbidity from ROP was an infrequent occurrence (18 of 266 premature infants--6.8%).

Female↗
PubMed2006

Kringle 5 of human plasminogen suppresses hepatocellular carcinoma growth both in grafted and xenografted mice by anti-angiogenic activity.

Plasminogen kringle 5 (K5), a proteolytic fragment of plasminogen, is an endogenous angiogenic inhibitor. We have previously shown that K5 inhibits ischemia-induced retinal neovascularization in a rat model. However, its anti-angiogenic potential and application in the treatment of neoplastic diseases have not been well investigated. Our present study was designed to test its effect on the neovascularization and growth of hepatocellular carcinoma, a typical hypervascular tumor. Recombinant human K5 was expressed in E. coli and purified by affinity chromatography. K5 inhibited proliferation and induced apoptosis of primary endothelial cells in dose-dependent manner, but no effect on pericytes from the same origin of endothelial cells, which suggested an endothelial cell-specific inhibition. Moreover, K5 had no effect on the proliferation and apoptosis of mouse HepA and human Bel7402 hepatoma cell lines even in the enhanced concentration range, which suggested K5 having no direct effect on tumor cells. Ventral injection of K5 significantly suppressed the tumor growth in graphed hepatocarcinoma mice model, which was established by injection of mouse HepA hepatoma cells. In xenografted hepatocarcinoma athymic mice model, which mimicked human tumors by injection of human Bel7402 hepatoma cells, K5 significantly suppressed the tumor growth. An average of 68% suppression of primary tumor growth was observed in the K5-treated mice compared with control group. K5 also inhibited intratumoral neovascularization in the two cancer models determined by micro vessel density (MVD) analysis. Injection of K5 significantly induced the cleavage of pro-caspase-3 in tumor tissues of grafted mouse model, which suggested K5 also induced apoptosis of tumor tissues and the decreased intratumoral microvascular density in K5 treated group may correlate with K5-induced endothelial cell apoptosis. These results suggest that tumor growth suppression of K5 depends on its anti-angiogenic activity and K5 could have therapeutic potential in hepatocellular carcinoma.

Angiogenesis Inhibitors↗
PubMed1998

Results of peripheral laser photocoagulation in pars planitis.

PURPOSE: To determine the effect of peripheral retinal laser photocoagulation (PLP) on visual acuity, intraocular inflammation, and other ocular findings, including retinal neovascularization in eyes with pars planitis. METHODS: A retrospective chart review of eyes with pars planitis that had undergone PLP. RESULTS: Twenty-two eyes in 17 patients with pars planitis had undergone treatment with PLP at 2 centers. The mean age at the time of treatment was 19.3 years. Following treatment, mean follow-up was 16.3 months (range, 6 to 37 months). Mean visual acuity was 20/60 preoperatively and 20/50 postoperatively. This level of improvement was not statistically significant (P > .10), but there was a statistically significant decrease in the use of corticosteroids between the preoperative examination and the last postoperative examination (86% versus 27%, P < .05). There was also a statistically significant decrease in vitritis at the last follow-up (P = .0008) and a decrease in neovascularization of the vitreous base (P = .03) and in clinically apparent cystoid macular edema (P = .02). Epiretinal membranes were noted in 23% of eyes preoperatively and in 45% of eyes postoperatively. Only one of these epiretinal membranes was considered to be visually significant. One eye developed a tonic dilated pupil, which slowly improved. CONCLUSIONS: Although the long-term natural history of clinical findings in pars planitis is not well documented, PLP appears to decrease the need for corticosteroids while stabilizing visual acuity. It also appears to decrease vitreous inflammation. PLP has few complications and should be considered in patients with pars planitis who are unresponsive or have adverse reactions to corticosteroids.

Adolescent↗
PubMed2000

PKC412--a protein kinase inhibitor with a broad therapeutic potential.

The staurosporine derivative PKC412 was originally identified as an inhibitor of protein kinase C (PKC) and subsequently shown to inhibit other kinases including the kinase insert domain receptor (KDR) (vascular endothelial growth factor receptor, VEGF-R2), the receptor of platelet-derived growth factor, and the receptor for the stem cell factor, c-kit. PKC412 showed a broad antiproliferative activity against various tumor and normal cell lines in vitro, and was able to reverse the Pgp-mediated multidrug resistance of tumor cells in vitro. Exposure of cells to PKC412 resulted in a dose-dependent increase in the G2/M phase of the cell cycle concomitant with increased polyploidy, apoptosis and enhanced sensitivity to ionizing radiation. PKC412 displayed a potent antitumor activity as single agent and was able to potentiate the antitumor activity of some of the clinically used cytotoxins (Taxol and doxorubicin) in vivo. The combined treatment of PKC412 with loco-regional ionizing irradiation showed significant antitumor activity against tumors which are resistant to both ionizing radiation and chemotherapeutic agents (dysfunctional p53). The finding that PKC412 is an inhibitor of the VEGF-mediated cellular signaling via inhibition of KDR and PKC in vitro is consistent with the in vivo inhibition of VEGF-dependent angiogenesis in a growth factor implant model. Orally administered PKC412 also strongly inhibited retinal neovascularization as well as laser-induced choroidal neovascularization in murine models. In summary, PKC412 may suppress tumor growth by inhibiting tumor angiogenesis in addition to directly-inhibiting tumor cell proliferation via its effects on PKC and/or other protein kinases. PKC412 is currently in Phase I clinical trials for treatment of advanced cancer as well as for the treatment of ischemic retinopathy.

Angiogenesis Inhibitors↗
PubMed2000

[The effects of photocoagulation on the electrical activity of the diabetic retina].

The aim of photocoagulation in diabetic retinopathy is to destroy ischaemic retina because this produces a vasogenic factor, responsible of neovascularization. Retinal burn reduces the number of photoreceptors and effects the transmission of nervous impulse in areas close to those coagulated. It is presumable therefore that electroretinographic parameters will be significantly modified after treatment. 23 diabetic patients where investigated, resulting 43 scotopic electroretinograms, 41 photopic electroretinograms and 46 flicker electroretinograms, each eye being considered separately. The statistic analysis showed significant alterations with laser treatment of the amplitudes of a and b waves in both scotopic and photopic conditions as well as diminished amplitude of the flicker test.

Aged↗
PubMed2002

[Ocular sarcoidosis].

Ocular involvement of sarcoidosis is frequent, and it is often the initial clinical manifestation of the disease. The most common ocular lesions include granulomatous uveitis associated with iris and trabecular nodules, string of pearl-type vitreous opacities, retinal paerivasculitis mainly affecting veins, and patchy retino-choroidal exudates. A half of the patients with typical ocular lesions suggestive of sarcoidosis did not show the systemic evidence, and they remained as sarcoidosis suspects. Risks of visual deterioration are secondary glaucoma, vitreous opacities, cystoid macular edema, and retinal neovascularization. Thirty-four % of the patients were treated with systemic corticosteroids, and some patients required other treatment such as methotraxate. Twenty-one% of the patients resulted in the poor visual acuity of less that 0.5.

Anti-Inflammatory Agents↗
PubMed2000

Detection of glutamate and gamma-aminobutyric acid in vitreous of patients with proliferative diabetic retinopathy.

PURPOSE: To study the levels of glutamate and gamma-aminobutyric acid (GABA) in vitreous of patients with proliferative diabetic retinopathy (PDR) and to investigate their roles in retinal ischemia. METHOD: Vitreous samples were collected from 25 patients (27 eyes) with PDR and 14 patients (14 eyes) with idiopathic macular hole. Glutamate and GABA detection were performed by high-performance liquid chromatography (HPLC). RESULTS: Patients with PDR had significantly higher concentrations of glutamate and GABA than the control group. The glutamate level has a significantly positive correlation with GABA level. CONCLUSION: Detection of glutamate and GABA in vitreous provides biochemical support for the mechanism and treatment of ischemic retinal damage in patients with PDR.

Diabetic Retinopathy↗
PubMed2003

[State-of-the-art of trans-vitreal surgery of the eye].

The modern condition of endo- and transvitreal surgery of the eye was demonstrated with regard for surgical approaches, technical outfit, expendables and medical preparations. Variants of clinical application of vitreal surgery methods at different pathologies of the vitreous body and retina, e.g. haemophthalmos of various etiologies, opacity of the vitreous body (including that of the uveal origin, proliferative diabetic retinopathy) diabetic macular edema, proliferative vitreoretinopathy of other etiologies (including complicated retinal detachments, posttraumatic vitreoretinopathy), complicated cataract extraction, macular pathology (including traction deformation of the retinal surface, senile macular holes and sub-retinal neovascular membranes) are discussed.

Eye Diseases↗
PubMed1992

[Idiopathic proliferative vitreoretinopathy. Activation of microglial cells as the deciding factor].

Mononuclear phagocytes are considered pacemakers in the pathogenesis of proliferative vitreoretinopathy (PVR), but their precise biological origin in preretinal PVR traction membranes has remained obscure. This study presents a combined immunohistochemical protocol for the detection of microglial cells, which was applied to 37 membranes of patients with idiopathic and traumatic PVR and with proliferative diabetic retinopathy (PDR). Microglial cells may be labeled by staining for LN-1, ricinus communis agglutinin-(RCA)-1, vimentin, HLA-DR-II, and nucleoside diphosphatase, but are negative for Leu-M1, Leu-M3, EBM-11, von Willebrand factor, CD22, cytokeratin, and glial fibrillary acidic protein (GFAP). Significant proliferation of microglial cells was found in idiopathic PVR while classical macrophages were typical of traumatic PVR. Only rarely were microglial cells detected in PDR. These findings bring into question previous concepts of the pathobiology of idiopathic PVR and support the hypothesis of idiopathic PVR as a specific disease entity.

Cicatrix↗
PubMed2003

[Macular dystrophies].

Macular dystrophies are a group of hereditary disorders of the macula occurring in children or young adults. The most frequent in France will be presented in detail: Best disease, Stargardt macular dystrophy, cone dystrophy, X-linked retinoschisis, pattern dystrophy, and malattia leventinese. Molecular biology studies have now mapped and identified the genes involved in these macular dystrophies. Analysis of the features of fundus examination will lead to further examinations such as fluorescein angiography, indocyanine green angiography, optical coherent tomography, electroretinography, or electrooculography, in order to confirm the diagnosis. We will also present the differential diagnosis of each of these macular dystrophies.

Adult↗