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Angiogenesis as a pathological process in the eye can lead to blindness. In the cornea, suppression of angiogenesis by anti-VEGF treatment is only partially effective while steroids, although effective in treating inflammation and angiogenesis, have broad activity leading to undesirable side effects. In this study, genome-wide expression was investigated in a suture-induced corneal neovascularization model in rats, to investigate factors differentially targeted by dexamethasone and anti- Vegf . Topical treatment with either rat-specific anti- Vegf , dexamethasone, or normal goat IgG (sham) was given to sutured corneas for 48 hours, after which  in vivo  imaging, tissue processing for RNA microarray, and immunofluorescence were performed. Dexamethasone suppressed limbal vasodilation (P < 0.01) and genes in PI3K-Akt, focal adhesion, and chemokine signaling pathways more effectively than anti- Vegf . The most differentially expressed genes were confirmed by immunofluorescence, qRTPCR and Western blot. Strong suppression of  Reg3g  and the inflammatory chemokines  Ccl2  and  Cxcl5  and activation of classical complement pathway factors  C1r, C1s ,  C2 , and  C3  occurred with dexamethasone treatment, effects absent with anti- Vegf  treatment. The genome-wide results obtained in this study provide numerous potential targets for specific blockade of inflammation and angiogenesis in the cornea not addressed by anti- Vegf  treatment, as possible alternatives to broad-acting immunosuppressive therapy.

Genome-wide expression differences in anti-Vegf and dexamethasone treatment of inflammatory angiogenesis in the rat cornea