Abstract
Purpose: :
Angiogenesis is a common wound-healing response in numerous diseases of the cornea that lead to blindness. Macrophage infiltration is an integral component of this inflammatory angiogenesis response, which is driven principally by the vascular endothelial growth factor (VEGF) family of proteins. Here we studied the effects of soluble VEGF receptors (sVEGFR-1, which blocks VEGF-A and VEGF-C, and monomeric sVEGFR-2, which blocks VEGF-C but not VEGF-A,) on macrophage recruitment and cornea angiogenesis in response to suture injury.
Methods: :
Two sutures were placed in the corneas of Balb/C mice. Recombinant sVEGFR-1/Fc chimera (or control IgG/Fc) or plasmid coding for sVEGFR-2 (or null plasmid) was injected into the corneal stroma. Angiogenesis and macrophage density were quantified by morphometric analysis of flat mount preparations stained with CD31 and Iba-1.
Results: :
sVEGFR-1/Fc dramatically reduced macrophage infiltration and angiogenesis compared to IgG/Fc. In contrast, overexpression of sVEGFR-2 did not impair either macrophage infiltration or angiogenesis compared to control plasmid.
Conclusions: :
These data suggest macrophage infiltration and angiogenesis in this model of injury-induced corneal angiogenesis are driven by VEGF-A and not VEGF-C.
Keywords: cornea: basic science • neovascularization