Purchase this article with an account.
X. Cai, L. L. Wong, S. Seal, J. F. McGinnis; Very Low Density Lipoprotein Receptor (VLDLr) Null Mice Exhibit Changes in Expression of Oxidative Stress Genes Which Are Reversed by Nanoceria. Invest. Ophthalmol. Vis. Sci. 2010;51(13):1424.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
The VLDLr-/- mouse, which develops retinal vascular lesions, choroidal neovascularization and retinal degeneration, is a model for a form of Age Related Macular Degeneration (AMD) called Retinal Angiomatous Proliferation (RAP). Because anti-oxidants have been shown to inhibit the development of the VLDLr phenotype and Nanoceria (cerium oxide nanoparticles) catalytically scavenge reactive oxygen species (ROS), we investigated whether the VLDLr null gene affects the expression of "oxidative stress-related" genes and if the Nanoceria prevent such changes.
Knocking out the VLDLr gene results in the upregulation, compared to WT controls, of a number of genes associated with protection from oxidative stress including Lactoperoxidase, Thioredoxin reductase, Glutathione peroxidase and Peroxiredoxin. Genes down regulated include Cathepsin, Dual oxigenase and Nucleoredoxin. Nanoceria application reversed such regulation.
Expression of key anti-oxidative stress genes in the VLDLr-/- retinas is not sufficient to prevent the retinal lesions. However, the Nanoceria by scavenging ROS, prevent the development of retinal vascular lesions and result in the downregulation of the anti-oxidative stress genes.
This PDF is available to Subscribers Only