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Isha Gupta, Subrata Das, Yang K Cho, Hironori Uehara, Xiaohui Zhang, Ashlie Bernhisel, Bonnie Archer, Balamurali Ambati; Vimentin knockdown reduces corneal scarring. Invest. Ophthalmol. Vis. Sci. 2014;55(13):5138.
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Wound induced corneal fibrosis can lead to permanent visual impairment. Keratocyte activation and differentiation play a key role in fibrosis, and vimentin, a major structural type III intermediate filament, is a required component of this process. The purpose of our study is to develop a non-viral therapeutic strategy for treating corneal fibrosis in which we target the knockdown of vimentin.
To determine the duration of plasmid expression in corneal keratocytes, we injected a naked plasmid expressing green fluorescent protein (GFP) (pCMV-GFP) into an unwounded mouse corneal stroma. To determine the duration of plasmid expression in a corneal wound injury model (full thickness corneal incision), we injected pCMV-GFP or pCMV.shRNA.vimentin into the wounded mouse corneal stroma.
GFP expression peaked between days 1 and 3 and had prominent expression for 15 days. In the corneal wound injury model, we found that the GFP positive cells demonstrated extensive dendritic-like processes that extended to adjacent cells, while the vimentin knockdown model showed significantly reduced corneal scarring.
These findings suggest that a non-viral gene therapeutic approach has potential for treating corneal fibrosis and reducing scarring.
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