The functional role of decorin in corneal neovascularization in vivo.

Abstract Our earlier decorin (Dcn) gene overexpression studies found that the targeted Dcn gene transfer into the cornea inhibited corneal angiogenesis in vivo using a rabbit model. In this study, we tested the hypothesis that anti-angiogenic effects of decorin in the cornea are mediated by alterations in a normal physiologic balance of pro- and anti-angiogenic factors using decorin deficient (Dcn −/−) and wild type (Dcn +/+) mice. Corneal neovascularization (CNV) in Dcn −/− and Dcn +/+ mice was produced with a standard chemical injury technique. The clinical progression of CNV in mice was monitored with stereo- and slit-lamp microscopes, and histopathological hematoxylin and eosin (HE p   0.05) compared to neovascularized Dcn +/+ mice corneas. These gene deficience studies carried with transgenic Dcn −/− mice revealed decorin's role in influencing a physiologic balance between pro-and anti-angiogenic factors in the normal and injured cornea. We infer that the functional deletion of Dcn promotes irregular corneal repair and aggravates CNV.