Disease relevance of Corneal Neovascularization

• Inhibition of corneal neovascularization by recombinant adenovirus mediated antisense VEGF RNA [1].
• CONCLUSION: This case report suggests that oral rofecoxib may trigger Stevens-Johnson syndrome, potentially causing symblepharons, corneal neovascularization and cicatricial ectropions [2].
• In vivo ABT-869 is effective orally in the mechanism-based murine models of VEGF-induced uterine edema (ED(50) = 0.5 mg/kg) and corneal angiogenesis (>50% inhibition, 15 mg/kg) [3].
• Trial lens fitting was performed 1 to 7 days later using a Burton Lamp. None of the patients developed keratitis, corneal neovascularization, or the sucked-on-lens syndrome [4].

High impact information on Corneal Neovascularization

• This cyclic oligosaccharide also augments the anti-angiogenic effect of angiostatic steroids against corneal neovascularization in rabbits when beta-cyclodextrin tetradecasulfate and a steroid are inserted into the cornea or applied topically as eyedrops [5].
• Soluble TweakR inhibits endothelial cell migration in vitro and corneal angiogenesis in vivo [6].
• Furthermore, the in vivo corneal angiogenesis induced by VEGF, but not by basic fibroblast growth factor, was selectively inhibited in mice treated with CsA systemically [7].
• It is sufficiently potent to effectively suppress basic fibroblast growth factor-induced corneal neovascularization after systemic administration in mice [8].
• Further supporting a role for MMP-9 in HSV-induced corneal angiogenesis was the observation that inhibition of MMP-9 with the specific inhibitor TIMP-1 resulted in reduced angiogenesis [9].

Chemical compound and disease context of Corneal Neovascularization

• To investigate the effects of D-penicillamine (D-Pen) on angiogenesis, we have studied the effects of this drug on in vitro proliferation of human endothelial cells (EC) and in vivo corneal neovascularization [10].
• Suramin, 200 mg/kg i.v., inhibited rat corneal angiogenesis induced by bFGF-impregnated polymers; addition of heparin stimulated angiogenesis and counteracted the inhibition of suramin [11].
• Endothelial migration and corneal angiogenesis are similarly inhibited by a TXA2 receptor antagonist, SQ29548 [12].
• In accord with these results, SC-68448 inhibited angiogenesis in vivo in a basic fibroblast growth factor-induced rat corneal neovascularization model [13].
• 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 [14].

Biological context of Corneal Neovascularization

• Our results imply that corneal-derived IL-8 may be important in corneal neovascularization, in particular, and that IL-8 may modulate wound healing in general [15].
• Plasminogen kringle 5 inhibits alkali-burn-induced corneal neovascularization [16].
• In combination-treated eyes, corneal re-epithelization was faster, corneal neovascularization was less severe, and intraocular pressure was not as severely elevated as in the saline or the Zn/DFO- or dexamethasone-alone groups [17].
• Downregulation of IRS-1 expression causes inhibition of corneal angiogenesis [18].
• Moreover, corneal injection of plasmid containing the cDNA for the soluble form of the VEGF receptor Flt-1 effectively prevented corneal neovascularization [19].

Anatomical context of Corneal Neovascularization

• PURPOSE: To examine the effects of 1alpha,25-dihydroxyvitamin D3 (1alpha,25[OH]2D3), a hormone that has immunosuppressive properties, on Langerhans cell (LC) migration and corneal neovascularization in mouse corneas [20].
• Recent observations suggest that collagenase from leukocytes may be a common mediator for prostaglandin E1 (PGE1)- and copper-induced corneal neovascularization [21].
• PURPOSE: To determine whether subunits of VEGF receptor-1 coupled with an endoplasmic reticulum retention signal can block hypoxia-induced upregulation of VEGF secretion in corneal epithelial cells and block murine corneal angiogenesis induced by corneal injury [22].
• MCP-1-induced angiogenesis in the cornea is associated with prominent recruitment of macrophages, whereas VEGF-A(121)-induced corneal angiogenesis is devoid of inflammatory cell recruitment [23].
• Suppression of corneal neovascularization by PEDF release from human amniotic membranes [24].

Gene context of Corneal Neovascularization

• Inhibition of rat corneal angiogenesis by a nuclease-resistant RNA aptamer specific for angiopoietin-2 [25].
• CONCLUSIONS: Corneal avascularity during development is redundantly regulated, shown by the fact that lack of the antiangiogenic factors TSP-1 and/or -2 resulted in no spontaneous corneal angiogenesis [26].
• TSP-1(-/-) had a significantly greater effect on induced corneal neovascularization than did TSP-2(-/-), with the opposite being the case in developmental iris angiogenesis (P < 0.01) [26].
• CONCLUSIONS: These data indicate that FasL is an important factor in controlling corneal neovascularization [27].
• A scavenger receptor, CD36, recognizes the active sequences in the type I repeats, and is required for the anti-angiogenic effects of TSP1 in the corneal neovascularization assay [28].

Analytical, diagnostic and therapeutic context of Corneal Neovascularization

• In another experiment (experiment II), epithelial closure was monitored with slit lamp biomicroscopy and fluorescein staining, and corneal neovascularization was confirmed by india ink perfusion, electron microscopy, and immunolocalization of CD31 and type IV collagen [29].
• METHODS: Resting limbal vessel surface area and density and extent of bFGF-induced corneal angiogenesis were determined in C57BL/6J, BALB/cJ, F1 intercross identical with C57BL/6J X 129S3/SvIM, and 129S3/SvIM mouse strains by quantitative three-dimensional reconstruction confocal microscopy [30].
• RESULTS: NG2 neutralizing antibody decreased corneal neovascularization in PC3 (P<0.0001), and LNCaP (P=0.0079) xenografts [31].
• Soft contact lenses cleaned and stored in thimerosal-containing solutions may produce an ocular inflammatory process and, if untreated, corneal neovascularization [32].
• We sought to determine if cyclosporine, which has been shown to suppress corneal allograft rejection, could also suppress corneal neovascularization induced by interleukin 2 [33].

References