Purchase this article with an account.
N. Singh, P. Jani, G. Liou, R. Kaur, N. Shah, J. Ambati, B. Ambati; Flt 2–4k Intraceptor Regresses Corneal Neovascularization by Apoptosis in Endothelial Cells . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1644.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Previously, we have demonstrated that Flt intraceptors can inhibit VEGF expression through endoplasmic sequestration and inhibit corneal neovascularization. In this study, we sought to determine whether flt2–4 k can regress corneal neovascularization and if it induces apoptosis.
FLT 2–4 domains were cloned into pCMV vector. On the 3’ end endothelial retention signal was attached. Mouse corneas were subjected to mechanical–alkali trauma. Two weeks later, either empty pCMV or pCMV.Flt24K was injected into mouse corneas into the stroma; 2 ug per eye were administered. One week later, corneas were harvested and sections were cut for immunohistochemistry. The sections were processed for Tunnel staining , using Apop Tag and CD 31 antibody and then analyzed with confocal microscopy. Neovascularization was quantified using the LSM–510 examiner.
Mean area of neovascularization on control corneas was 55.0%, whereas corneas treated with pCMV.Flt24K was 32.5% (p=0.03). On immunohistochemistry using TUNEL staining, apoptosis was significantly more common in corneal vascular endothelial cells in corneas treated with pCMV.Flt24K.
FLT2–4 k can regress corneal neovascularization, and its mechanism likely involves apoptosis in endothelial cells.
This PDF is available to Subscribers Only