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J.S. Zigler, C. Zhang, M. Arora, S.L. Hose, P.L. Gehlbach, M.F. Goldberg, D. Sinha; Upregulation of Lens VEGF in a Rat Model With Persistent Hyaloid Vasculature . Invest. Ophthalmol. Vis. Sci. 2005;46(13):2902.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: A spontaneous mutation (Nuc1) in the Sprague–Dawley rat causes a number of eye–specific pathologies, including persistent fetal vasculature (PFV). Since the level of vascular endothelial growth factor (VEGF) in the lens may be involved in the normal regression of the fetal vasculature, we have investigated VEGF expression in the Nuc1 lens. Methods: Expression of VEGF in the lens of Nuc1 and age–matched wildtype rats was assessed by western blotting with VEGF specific antibodies. Localization of VEGF expression was determined immunohistochemically on frozen sections of eyes from Nuc1 and wildtype rats. Results: Immunohistochemical analysis of Nuc1 and wildtype eyes from rats 5 weeks of age using VEGF specific antibodies revealed little or no detectable signal in wildtype lens whereas strong immunofluorescence was present in the lens tissue (both fibers and epithelial cells) of Nuc1. At this stage the fetal vasculature has completely regressed in the normal eye, but in Nuc1 it remains intact. Western blotting confirmed that VEGF is present at much higher levels in the mutant lens than in the wildtype lens and also indicated that in Nuc1 multiple isoforms of VEGF are expressed. Conclusions: The data are consistent with the idea that persistence of the fetal vasculature of the eye may be associated with elevated levels of VEGF in the lens. Additional work is needed to establish that a cause and effect relationship exists between these two events. The Nuc1 model provides opportunities to investigate this and other aspects of the pathophysiology of PFV.
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