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B. K. Ambati, P. D. Jani, N. Singh, C. Jenkins, S. Raghava, M. Yun, S. Sundaram, A. Mayo, R. Caldwell, U. B. Kompella; Nanoparticles Sustain Extended-release of Flt Intraceptors in the Cornea and Can Inhibit Injury-induced Corneal Angiogenesis. Invest. Ophthalmol. Vis. Sci. 2007;48(13):3197.
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To determine whether long-term expression of intraceptors can be achieved using plasmid-albumin nanoparticles and whether nanoparticles can inhibit and regress murine corneal neovascularization induced by mechanical-chemical trauma
Albumin nanoparticles encapsulating pCMV.Flt23K were developed as a lyophilized product that is easily redispersed in an aqueous medium. Nanoparticles were injected into the corneas of uninjured Balb/C mice and observed for toxicity for 3 weeks. Entry of nanoparticles into corneal cells was demonstrated through transmission electron microscopy and confocal imaging. Naked pCMV.Flt23K, nanoparticles encapsulating pCMV.Flt23K, or empty pCMV nanoparticles were injected into uninjured mouse corneas. These corneas were subjected to mechanical-alkali trauma 3 weeks after injection.
Nanoparticles were non-toxic to the cornea and entered into corneal keratocyte cytoplasm. They persisted for at least 4 weeks in the cornea. Nanoparticles expressed effective intraceptor levels for at least 5 weeks and reduced corneal neovascularization by approximately 40% (p=0.035) at 5 weeks post-administration.
Albumin nanoparticles are not toxic to the cornea and can express intraceptors for extended periods of time, which are effective in suppressing injury-induced corneal neovascularization.
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