In patients with age-related macular degeneration (AMD), choroidal neovascularization is the
major cause of severe visual loss. In these patients, the persistence of neovascular growth
despite vascular endothelial growth factor-A blockage needs the discovery of new endothelial
cell targets. The glycoprotein CD93, highly expressed in activated endothelial cells, has been
recently involved in the regulation of the angiogenic process both as transmembrane and
soluble protein.
Choroidal neovascular membranes from patients affected by AMD were examined by
immunofluorescence using anti-CD93 and anti-von Willebrand factor antibodies. Blood
vessels within intraocular and extraocular neoplasias were used as controls for CD93
expression. All choroidal neovascular membranes displayed strong CD93 staining in the von
Willebrand factor-positive endothelial cells, consistently with the analyses showing a high
colocalization coefficient in the blood vessels. Intraocular and extraocular tumor vessels
showed similar results, whereas the normal choroid displayed blood vessels with only faint
CD93 staining. Additionally, the concentration of soluble CD93 was determined in the
aqueous humor of patients affected by naïve neovascular AMD by enzyme-linked
immunosorbent assays. Age-matched cataract patients served as controls. Soluble CD93
was significantly increased in the aqueous humor of naïve neovascular AMD patients and
tended to decrease after treatment with an antiangiogenic drug. In conclusion, both
transmembrane and soluble CD93 are overexpressed in patients with neovascular AMD,
indicating that CD93 may represent a potential new antiangiogenic target in the treatment of
choroidal neovascularization.