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At least 19 recordsLinked to original sources
PubMed1995

Topical and subcutaneous alpha-interferon fails to suppress corneal neovascularization.

Corneal neovascularization is a potentially blinding complication of a variety of corneal disorders. alpha-Interferon has been shown to inhibit endothelial cell migration and proliferation. It has been used successfully in the treatment of pediatric pulmonary hemangioma and hairy cell leukemia. This study was undertaken to evaluate the effect of topical and subcutaneous (s.c.) alpha-interferon on corneal neovascularization. Corneal neovascularization was induced in 40 male New Zealand white rabbits by placing silk sutures (7.0) bilaterally in each rabbit eye at the 3 and 9 o'clock positions of the cornea, 3 mm from the limbus. Animals were randomized into two main treatment groups for topical (group 1) and s.c. (group 2) administration of interferon. Group 1 (n = 24) was then randomized into four subgroups and treated daily with topical doses of (a) rabbit specific alpha-interferon; (b) alpha-interferon plus 1% prednisolone acetate; (c) 1% prednisolone acetate; and (d) buffered phosphate control. Group 2 (n = 16) was randomized into two subgroups that received s.c. injections every other day of (a) alpha-interferon and (b) phosphate buffer. Rate of corneal neovascularization was documented photographically, with the end-point being the arrival of vessels at the suture for each group. The results of this study indicated that at the concentration and dosing regimens we used, neither topical nor s.c. alpha-interferon inhibits the rate of corneal vascular growth significantly when compared with our phosphate buffered solution control group (p = 0.88 and p = 0.84, respectively). Prednisolone acetate appeared to be the most effective in inhibiting corneal neovascularization (p = 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Topical↗
PubMed1993

Biomicroscopic and histopathologic observations after corneal laser photocoagulation in a rabbit model of corneal neovascularization.

Corneal neovascularization complicates many anterior segment diseases. Corneal laser photocoagulation using yellow light (577 nm) has been shown to reduce corneal neovascularization. No histopathologic studies of the effects of this treatment on the eye have been reported, however. Target (cornea) and nontarget (iris, lens, retina, and choroid) ocular tissue were studied 1, 24, and 48 h and 5 days after yellow dye corneal laser photocoagulation in a rabbit model of corneal neovascularization. Biomicroscopic examination of the corneas revealed intracorneal hemorrhage in five of 24 (21%) eyes of nonpigmented rabbits. Faint lenticular opacities were observed in two eyes of pigmented rabbits 24 h after laser treatment. Histopathologic examination revealed increased cellularity (neutrophils) (p < 0.005) in the cornea, increasing from 1 h after treatment, peaking 24 h later, and persisting past 5 days. Distortion of the corneal lamellae by red blood cells occurred in eyes in which intracorneal hemorrhage developed. These results indicate that corneal laser photocoagulation using yellow light is a relatively safe procedure for reducing corneal neovascularization.

Animals↗
PubMed1989

Promotion of graft survival by photothrombotic occlusion of corneal neovascularization.

Corneal neovascularization may reduce the success of penetrating keratoplasty. Photothrombosis using intravenous rose bengal and argon laser irradiation has shown promise for occluding corneal vessels. It is therefore conceivable that photothrombosis can improve the graft survival in vascularized corneas. Using intracorneal 7-0 silk sutures as the stimuli, corneal neovascularization was induced in 1 eye each of 19 New Zealand white rabbits. Eleven eyes received photothrombosis. Successful occlusion with subsequent regression was verified by corneal fluorescein angiography. Three were assigned for observation. Six of 8 eyes receiving grafts from an outbred rabbit donor after photothrombosis remained clear during 6.5 to 18.5 weeks of follow-up, while vascularization and opacity occurred in 7 of 8 control eyes without photothrombosis. These results indicate that prior photothrombotic occlusion of corneal vessels can significantly improve graft survival in this experimental model and may have clinical applications.

Animals↗
PubMed2001

Corneal neovascularization.

Corneal neovascularization (NV) is a sight-threatening condition usually associated with inflammatory or infectious disorders of the ocular surface. It has been shown in the field of cancer angiogenesis research that a balance exists between angiogenic factors (such as fibroblast growth factor and vascular endothelial growth factor) and anti-angiogenic molecules (such as angiostatin, endostatin, or pigment epithelium derived factor) in the cornea. Several inflammatory, infectious, degenerative, and traumatic disorders are associated with corneal NV, in which the balance is tilted towards angiogenesis. The pathogenesis of corneal NV may be influenced by matrix metalloproteinases and other proteolytic enzymes. New medical and surgical treatments, including angiostatic steroids, nonsteroidal inflammatory agents, argon laser photocoagulation, and photodynamic therapy have been effective in animal models to inhibit corneal NV and transiently restore corneal "angiogenic privilege."

Angiostatins↗
PubMed1995

[A morphological study of experimental corneal neovascularization].

Corneal neovascularization (CNV) was induced by alkali burn injuries in 20 rabbit corneas. The process of CNV was observed with biomicroscopy in vivo and histologically by light and electron microscopy. At 8 hours after injury, an obvious acute inflammatory response as evidenced by infiltration of neutrophils had already occurred in the pericorneal limbal area. Many neutrophils in the extravascular space contained abundant intracytoplasmic phagolysosomes. The vascular sprouts appeared 2 days after injury. The infiltration of neutrophils and their debris were visible around newly formed blood vessels in the cornea. The results suggest that there be the participation and an inductive action of neutrophils in the pathogenesis of CNV.

Animals↗
PubMed2001

[Standardized semiquantitative analysis of corneal neovascularization using projected corneal photographs--pilot study after perforating corneal keratoplasty before immune reaction].

BACKGROUND: A semiquantitative scheme for analysis of corneal neovascularization using projected corneal photographs is demonstrated and tested in a pilot study to analyze occurrence of corneal neovascularization in patients after perforating keratoplasty which subsequently developed transplant rejection. METHODS: Corneal photographs on the slit lamp with diffuse frontal illumination were obtained in a standardized technique. Slides were projected with 100 x magnification and analyzed twice with a 2 months interval. Corneal vessels were graded by two independent observers in each of 12 corneal sectors in a standardized fashion (grade 0: no vessels beyond limbus, 1: vessels between limbus and outer end of a double-running diagonal suture; 2: vessels between outer suture end and graft-host junction; 3: vessels reaching graft-host junction; 4: vessels within donor cornea). All patients with endothelial graft rejection of the prospective Erlangen non-high-risk keratoplasty study were included in a pilot study (1/1997-6/2000: 13 of 325; 4%). One patient without photographs available was excluded. Corneal photographs taken prior to surgery (n = 10), at the last 3 monthly-routine control before (10), at rejection episode (12) and one year later (10) were evaluated for corneal neovascularization. RESULTS: Interobserver correlation at the two assessments was 0.79 and 0.86 (Kendall's Tau B). Correlation between the assessments at the two analyses 2 months apart was 0.8. New vessels with diameter up to 6 microns can be detected. 8 of 12 analyzed patients (67%) with immune reaction after keratoplasty developed corneal neovascularization within 1 year after operation prior to transplant rejection in at least one corneal sector (2.1 +/- 1.9 sectors; 1-6). At time of rejection, new vessels reached the graft-host junction in 2 patients, in 1 patient vessels grew into the donor cornea, whereas in 8 the vessels were seen beyond the outer suture end without reaching host-graft junction (grade I: 1 patient). New vessels usually pointed to the outer suture ends of the double-running suture. CONCLUSIONS: Development of corneal neovascularization e.g. after keratoplasty can be assessed reliably using projected slides of corneal photographs at 100 x magnification. This method has the advantage of being more objective, precise and available compared to simple evaluation at the slit lamp. Postkeratoplasty corneal neovascularization seems to be common in non-high-risk eyes later developing transplant rejection. However, new vessels usually do not reach the host-graft junction. Whether neovascularization after keratoplasty demonstrates a risk factor for subsequent transplant rejection remains to be analyzed in a greater study.

Cornea↗
PubMed2000

Treatment of corneal neovascularization with dietary isoflavonoids and flavonoids.

The purpose of this study was to investigate the use of dietary isoflavonoids and flavonoids for the treatment of ocular neovascularization. Corneal blood vessels were induced by intrastromal implantation of pellets containing bFGF. Isoflavonoids and flavonoids (Genistein, Fisetin and Luteolin) were dissolved in a microemulsion to increase bioavailability and applied topically in concentrations between 0.5 and 1 ng ml(-1). Corneal neovascularization was quantified under the microscope. In comparison to control eyes, all three substances significantly inhibited corneal neovascularization (P < or = 0.05). Fisetin had the strongest effect followed by Genistein and Luteolin. No significant topical side effects were observed. We concluded that the isoflavonoid Genistein and two structurally related flavonoids are potent inhibitors of corneal angiogenesis in vivo. The wide distribution of the flavonoids in the plant kingdom together with the presented results suggests that flavonoids may contribute to the preventive effect of a plant-based diet on neovascular disease of the eye.

Administration, Topical↗
PubMed2006

The role of PDGF receptor inhibitors and PI3-kinase signaling in the pathogenesis of corneal neovascularization.

PURPOSE: Corneal neovascularization remains an unsolved therapeutic problem. Platelet-derived growth factor (PDGF) is directly linked to vessel formation and stabilization. This study was undertaken to elucidate the mechanisms by which PDGF exerts its effects on corneal angiogenesis. METHODS: Corneal neovascularization was induced in C57 mice by removal of the limbal epithelium. When mature vessels appeared after 7 days, mice were treated with the PDGF receptor-beta inhibitor AG 1296 or the phosphatidylinositol 3-kinase (PI3-K)-inhibitors wortmannin and LY294002, respectively, using an intraperitoneally implanted miniosmotic pump. At day 14 after scraping, corneas of treated and untreated (control) mice were dissected and immunostained with FITC-CD31 antibody for endothelial cells and with Cy3-SMA (smooth muscle actin) for pericytes. VEGF (vascular endothelial growth factor), ang1/2 (angiopoietin 1 and 2), and PDGF mRNA levels of treated and untreated corneas were determined by real-time RT-PCR. RESULTS: Mice treated with the PDGF inhibitor AG 1296 showed an inhibition of corneal neovascularization of 21.1% and a reduction of pericytes of 52% in the newly formed vessels compared with untreated animals. VEGF, ang1, ang2, and PDGF mRNA expression was reduced in the corneas of AG 1296-treated mice compared with the respective control. Treatment with the PI3-K inhibitors wortmannin and LY29002 had similar effects, inducing a decrease in corneal neovascularization and a reduction of VEGF, ang1, ang2, and PDGF mRNA levels. CONCLUSIONS: Inhibition of the PDGF signal pathway results in loss of pericytes and a reduction in vessel density in the neovascularized cornea that correlates with reduced expression of PDGF, ang1/2, and VEGF mRNA. Furthermore, PI3-K was shown to be involved in the regulation of VEGF, ang1, and PDGF, as the PI3-K inhibitors wortmannin or LY294002 had similar effects. Because PDGF is a known stimulus for PI3-K activation, it can be postulated that the observed decrease in VEGF, ang1/2, and PDGF mRNA levels on administration of the PDGF inhibitor is caused by the decreased activation of the PI3-K signaling cascade.

Androstadienes↗
PubMedDate not supplied

Comparison of yellow dye, continuous wave Nd:YAG, and argon green laser on experimentally induced corneal neovascularization.

BACKGROUND: Corneal neovascularization is generally undesirable because it can lead to corneal scarring, lipid deposits, and corneal graft failure. To eliminate these vessels, several techniques are available including laser photocoagulation. METHODS: This prospective study was designed to compare the effectiveness of three laser wavelengths (continuous wave Nd:YAG, 1064 nm; argon green 514 nm; and yellow dye, 570 nm) to obliterate experimentally induced corneal neovascularization in the rabbit. Corneal vascularization was created in 12 rabbits by placing 7-0 silk sutures through two quadrants of the cornea. Once neovascularization was complete, the suture was removed and one of the three lasers was applied to occlude vessels at one of the neovascular sites. The other site was used as a control. RESULTS: The yellow wavelength, when compared with the green required fewer exposures to occlude corneal vessels. At no time during observation was any laser more effective than the control. In the continuous wave Nd:YAG group, tissue necrosis was needed to achieve closure of vessels. CONCLUSIONS: Yellow and green laser light are equally effective in eliminating the corneal vessels. Continuous wave Nd:YAG, as used here, appears to be a poor choice.

Animals↗
PubMed2002

Corneal neovascularization after nonmechanical versus mechanical corneal trephination for non-high-risk keratoplasty.

PURPOSE: To analyze the influence of mechanical versus nonmechanical trephination of donor and host corneas on superficial, peripheral corneal neovascularization occurring after non-high-risk keratoplasty. METHODS: Patients of the prospective Erlangen non-high-risk keratoplasty study with standardized corneal photographs taken preoperatively and 1 year later were analyzed (n = 184). Slides of these photographs were projected (magnification x100) and corneal vessels graded in a standardized semiquantitative fashion into five categories with regard to limbus, sutures, and host-graft junction in each of 12 corneal sectors. Degree (total increase of grades in the 12 sectors) and maximal extent of corneal neovascularization (maximal centripetal extension of blood vessels) were analyzed. In 32 patients mechanical (17%) and in 152 nonmechanical trephination of host and donor tissue was performed (193-nm excimer laser, 83%). Statistical analysis was done using Fisher's exact and Mann-Whitney test. RESULTS: Corneal neovascularization within the first postoperative year was lower in the nonmechanical [73 of 152 (48%)] compared with mechanical trephination group [24 of 32 (75%); p< 0.01; Mann-Whitney test]. Maximal extent of neovascularization (i.e., vessels reaching the interface or growing beyond) was not yet significantly different between nonmechanical (8%) and mechanical (17%) trephination (p = 0.074). CONCLUSIONS: Nonmechanical trephination using the 193-nm excimer laser in non-high-risk keratoplasties might reduce corneal neovascularization occurring within the first postoperative year. This indicates that in the non-high-risk setting, development of postoperative corneal neovascularization may be affected by the trephination technique and subsequent wound-healing response.

Aged↗
PubMed2005

Inhibitory effect of triamcinolone acetonide on corneal neovascularization.

BACKGROUND: Corneal neovascularization (NV) plays an important role in the pathogenesis of corneal disorders. Recently, triamcinolone acetonide (TA) has been reported as a potential treatment for ocular angiogenesis. However, there are no reports on the inhibitory effect of TA on the corneal NV. METHODS: Triamcinolone acetonide (2 mg) was administered to four rabbits' eyes by a subconjunctival injection immediately after a basic fibroblast growth factor (bFGF)-pellet was placed into the cornea. As a control, four eyes received an injection of distilled water. Four weeks later, the inhibition of corneal NV was evaluated as the percentage ratio of the vessel invasion area to the area that was sandwiched between the pellet and the limbus cornea. To identify the characteristic appearance of new corneal vessels, the control cornea was examined by using the antibody of vascular endothelial growth factor (VEGF). To confirm TA concentration in TA-treated corneas, the TA level was measured using high-performance liquid chromatography. RESULTS: Neovascularization from the limbus to the pellet was detected in control eyes 4 weeks after the bFGF pellet implantation. TA-treated eyes demonstrated the inhibition of the neovascular response to the pellet. The severity of NV as compared between control and TA-treated eyes was statistically significant (P<0.05). Morphologically, new vessel growth was shown in the control cornea, and endothelial cells of new vessels were positively stained with the antibody of VEGF. TA concentration in TA-treated corneas at 2 weeks showed 63.5+/-42.8 microg/g (n=4, mean +/- SD), while TA was not detected in control and TA-treated corneas at 4 weeks. The level of TA was effectively maintained for at least 2 weeks after the subconjunctival injection. CONCLUSION: We have demonstrated that subconjunctival TA administration inhibited rabbit corneal NV. This agent may prove useful in the treatment of corneal angiogenic disorders.

Animals↗
PubMed2006

Effects of corneal neovascularization on the manifestations of Avellino corneal dystrophy (granular corneal dystrophy type II).

PURPOSE: To evaluate the corneal deposits of Avellino corneal dystrophy (ACD) in patients with corneal neovascularization from pterygium or phthisis bulbi as a way of understanding the pathogenesis of ACD. METHODS: Five patients with ACD with pterygium, 10 patients with ACD (age >50 years) without pterygium, 1 patient with ACD with phthisis bulbi with corneal neovascularization, and 1 patient with ACD with phthisis bulbi without corneal neovascularization were examined. The corneal deposits of all patients were assessed by slit-lamp examination and reviewed with biomicroscopic photographs. The distance between the limbus and the nearest corneal opacities was measured. RESULTS: In eyes with vascularized nasal pterygia, there was a granule-free zone adjacent to the advancing edge of the pterygium so that the distance between the nasal limbus and the most nasally located granule exceeds that of the distance between the limbus and the closest granule elsewhere on the cornea. In patients with ACD with phthisis bulbi, no granular deposits were observed in the cornea with neovascularization, but there were deposits in the cornea without neovascularization. CONCLUSION: Corneal neovascularization prevents the deposition of corneal opacities in patients with ACD.

Adult↗
PubMed2005

Deep corneal neovascularization after implantation with intrastromal corneal ring segments.

PURPOSE: To demonstrate the development of deep corneal neovascularization after intrastromal corneal ring segment (ICRS) implantation, and to demonstrate complete regression after treatment with surgical removal and anti-inflammatory therapy. DESIGN: Observational case report. METHODS: A 29-year-old man developed deep stromal neovascularization after ICRS implantation for post-laser-assisted in situ keratomileusis ectasia that was not associated with the surgical wound. RESULTS: After surgical removal of the ICRS and treatment with topical prednisolone acetate 1.0% and cyclosporine A 1.0%, complete vessel regression occurred in 2 weeks. CONCLUSIONS: ICRS can induce deep corneal neovascularization that is not associated with the surgical wound. Surgical removal of the intrastromal ring and treatment with topical anti-inflammatory agents can induce vessel regression.

Adult↗
PubMed1993

Treatment of corneal neovascularization with argon laser.

Corneal neovascularization, which is associated with complications in corneal diseases, can cause lipid deposit, decreasing vision, and graft rejection after penetrating keratoplasty (PKP). Corneal laser photocoagulation using an argon laser or yellow dye laser for ablation of corneal neovascularization has been described. We performed corneal argon laser photocoagulation (CALP) in two male patients with corneal neovascularization after herpetic keratitis. One PKP was performed after CALP and restored good vision with no rejection of the graft during an 8 month follow-up period. In the other case we observed visual improvement and no recurrence of corneal neovascularization after CALP.

Adult↗
PubMed1993

Effectiveness of corneal neovascularization photothrombosis using phthalocyanine and a diode laser (675 nm).

We used chloroaluminum sulfonated phthalocyanine as a photo-sensitizer and a diode laser as a light source for induction of photothrombosis of corneal neovascularization. Corneal neovascularization was induced in 1 eye of each of 10 New Zealand white rabbits using intrastromal 6.0 silk sutures. After the intravenous injection of phthalocyanine in a dose of 4 mg per kg of body weight, photothrombosis was carried out using a diode laser emitting at 675 nm. The animals were followed up by both fluorescein angiography and slit-lamp photography for up to three months. At the end of the follow-up period the eyes were prepared for histology. After photothrombosis, thrombus formation was induced within new vessels demonstrating histological characteristics of both arterioles and venules. Most of the vessels disappeared or remained closed during the follow-up period. Recanalization of some of the thrombosed vessels occurred within the first 20 days after the operation. The combination of phthalocyanine and a 675 nm diode laser is effective for the induction of photothrombosis of corneal neovascularization.

Aluminum↗
PubMed1997

Role of protein tyrosine phosphorylation in rat corneal neovascularization.

BACKGROUND: Recent studies have suggested that tyrosine kinase pathways that are activated by angiogenic growth factors may play a role in corneal neovascularization. METHODS: Corneal neovascularization was induced in rat corneas by chemical cauterization. At 6, 24, 48, 96, and 168 h after chemical cauterization the rat corneas without the corneal epithelium were prepared for gel electrophoresis. Total protein profiles of the corneal samples were examined by staining gels with Coomassie brilliant blue. Tyrosine-phosphorylated proteins, three angiogenic growth factors (basic fibroblast growth factor, vascular endothelial growth factor, and platelet-derived growth factor-B chain), and three intracellular signal proteins in the tyrosine kinase pathways (phospholipase C gamma, SHC, and mitogen-activated protein kinase) in the corneal samples were examined by western blot analysis. A topical treatment of genistein eye drop (5 mg/ml) was used for inhibition of corneal neovascularization after chemical cauterization in rats. RESULTS: In total protein profiles, three bands in the corneal samples were increased after cauterization. Overall tyrosine-phosphorylated proteins and all three angiogenic growth factors increased with progression of corneal neovascularization. The tyrosine-phosphorylated forms of three intracellular signal proteins were also increased after cauterization. Treatment with topical genistein was effective in inhibiting corneal neovascularization in rats. CONCLUSION: Protein tyrosine phosphorylation was involved in inflammation-induced corneal neovascularization. Tyrosine kinase inhibitors may have utility as inhibitors of corneal neovascularization.

Animals↗
PubMed2005

[Inhibition of rat corneal neovascularization by inhibitor of nuclear factor-kappaB].

OBJECTIVE: To observe the effects and mechanism of pyrrolidine dithiocarbamate (PDTC) on inhibiting corneal neovascularization. METHODS: The corneal neovascularization was induced by alkali burn in 48 Sprague-Dawley rats. The rats were randomly divided into 4 groups, 12 rats in each group. The PDTC eye drops with different concentrations were applied four times daily during days 0 - 28 in each group: 0.5 mg/ml in group A, 1 mg/ml in group B, 2 mg/ml in group C and 0.9% sodium chloride in group D (control). The development of corneal neovascularization and corneal opacity were observed daily with slit lamp. Corneas were excised at day 4 and 28 (six eyes were selected randomly in each group per time) for histopathological examinations. The expression of nuclear factor-kappaB (NF-kappaB) in the cornea was examined by Western Blot. RESULTS: The corneal neovascularization area in groups B and C were significantly smaller than that in the control group (P < 0.01). The corneal opacification and inflammation level in groups B and C were also lower than that in the control group. No significant difference was found in corneal neovascularization areas and corneal opacification levels between group A and group D (P > 0.05). The activity of NF-kappaB in groups B and C was significantly lower than that of group D. No significant difference in NF-kappaB could be detected between group A and group D. CONCLUSION: Topical application of PDTC has significant effects on the inhibition of activation of NF-kappaB and cornea neovascularization.

Animals↗
PubMed2005

Lipid-mediated delivery of brain-specific angiogenesis inhibitor 1 gene reduces corneal neovascularization in an in vivo rabbit model.

Corneal neovascularization, which occurs in many pathologic states of the cornea, reduces the visual acuity. Recently, we found that the extracellular region of brain-specific angiogenesis inhibitor 1 (BAI1-ECR) has antiproliferative activity through functional blocking of alpha(v)beta(5) integrin in endothelial cells. In this study, we investigated the effects of lipid-mediated subconjunctival injection of the BAI1-ECR gene on corneal angiogenesis induced by epithelial debridement by heptanol in the rabbit. When a pEGFP-BAI1-ECR plasmid was given subconjunctivally 1 week after epithelial debridement, green fluorescence was detected in the corneal stroma with expression persisting for 7 days. To test the effect of BAI1-ECR on neovascularization, rabbits were injected with the BAI1-ECR gene or empty vector two or three times at 1-week intervals beginning 1 week after debridement. When measured with biomicroscopy at 1 or 2 weeks after two weekly injections, BAI1-delivered eyes had significantly less neovascularized corneal area than vector-injected ones in both time periods. Similar microscopic results were obtained after three weekly injections of BAI1-ECR. In quantitative histological examination, the BAI1-receiving eyes showed significantly less neovascular area and number of vessels than vector-injected ones. Also, after two weekly injections, BAI1-delivered eyes had decreased neovascularized corneal area equivalent to that of anti-VEGF antibody-injected ones. These results indicate that BAI1-ECR gene delivery effectively reduces experimental corneal neovascularization and suggest that the BAI1-ECR protein can be used as an angiogenesis suppressor in the eye.

Angiogenic Proteins↗