Angiogenesis, the growth of new blood vessels, is a fundamental biological process that plays a central role in the pathogenesis of cancer, diabetic retinopathy, and macular degeneration, in which vascular overgrowth is detrimental. In the eye, vision-threatening angiogenesis can be caused by diabetes mellitus, age-related macular degeneration, rejection of corneal transplants, chemical burns, infections such as trachoma, Stevens-Johnson syndrome, and other disorders.1 The cornea is normally avascular, to permit optimal visual clarity. However, in pathologic conditions, neovascularization can occur, compromising clarity and thus vision. Corneal neovascularization is a central feature in the pathogenesis of many blinding corneal disorders, and a major sight-threatening complication in corneal infections and chemical injury and after keratoplasty, in which neovascularization adversely affects the corneal transplant’s survival.1 New approaches to diminishing or completely preventing corneal neovascularization are greatly needed.
Vascular endothelial growth factor (VEGF) has been demonstrated to be a key mediator of angiogenesis in many models.2–13 In the cornea, the angiogenic process has been shown to be driven by increased secretion of VEGF.2 Although several studies have shown that VEGFR-2/KDR is the signal transducer for VEGF-induced mitogenesis, chemotaxis, and cytoskeletal reorganization and thus is the principal receptor involved in angiogenesis,3,14 –16 VEGFR-1/Flt-1 has a 10-fold higher binding affinity. Domain deletion studies have shown that a subunit construct of domains 2 to 3 binds VEGF with near wild-type affinity and that domain 1 serves as a secretion signal sequence. Domain 4 is also thought to participate somewhat in VEGF binding.
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