VEGF-A stimulates lymphangiogenesis and hemangiogenesis in inflammatory neovascularization by recruiting macrophages. In a novel model of inflammatory neovascularization in the cornea, VEGF Trap, a receptor-based fusion protein that neutralizes VEGF-A, completely inhibited both hemangiogenesis and lymphangiogenesis. Transgenic mice expressing only VEGF-A isoforms 144/164 or 188 showed reduced lymphangiogenesis and hemangiogenesis. Depletion of bone marrow-derived cells or local depletion of macrophages in the cornea also inhibited both processes. Macrophages in inflamed corneas release VEGF-C and VEGF-D, which are essential for lymphangiogenesis. These findings suggest that VEGF-A recruits monocytes/macrophages to supply signals that amplify pathological hemangiogenesis and lymphangiogenesis.VEGF-A stimulates lymphangiogenesis and hemangiogenesis in inflammatory neovascularization by recruiting macrophages. In a novel model of inflammatory neovascularization in the cornea, VEGF Trap, a receptor-based fusion protein that neutralizes VEGF-A, completely inhibited both hemangiogenesis and lymphangiogenesis. Transgenic mice expressing only VEGF-A isoforms 144/164 or 188 showed reduced lymphangiogenesis and hemangiogenesis. Depletion of bone marrow-derived cells or local depletion of macrophages in the cornea also inhibited both processes. Macrophages in inflamed corneas release VEGF-C and VEGF-D, which are essential for lymphangiogenesis. These findings suggest that VEGF-A recruits monocytes/macrophages to supply signals that amplify pathological hemangiogenesis and lymphangiogenesis.