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R. L. Gendron, T. Islam, H. Paradis; The Effects of Tubedown on Permeability of Endothelial Cells. Invest. Ophthalmol. Vis. Sci. 2007;48(13):1727.
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Tubedown is a mammalian homologue of the N-terminal acetyltransferase subunit NAT1 of Saccharomyces cerevisiae and copurifies with an acetyltransferase activity. Previous studies of the expression level of Tubedown demonstrated a suppression of Tubedown in the retina of patients with proliferative diabetic retinopathy. Conditional endothelial suppression of Tubedown in a transgenic mouse model leads to proliferative neovascular retinopathy and structural changes in retinal blood vessels. It has been shown that structural changes in retinal blood vessels in proliferative diabetic retinopathy are accompanied by changes in the permeability of retinal endothelial cells. Therefore, in the current study we investigated the functional role of Tubedown expression on permeability of retinal endothelial cells.
An in vitro assay to measure permeability of endothelial monolayers to FITC-labeled Albumin was performed using stable transfectant clones of RF/6A retinal endothelial cells harboring an antisense Tubedown cDNA construct and negative control clones.
Our results indicate a significant increase in the permeability of monolayers of Tubedown knockdown RF/6A clones to FITC-labeled Albumin compared to control clones.
Our results suggest that expression of Tubedown is required for the regulation of retinal endothelial permeability. Since an increase in the permeability of retinal endothelial cells has been implicated in contributing to the pathological neovascularization seen in proliferative diabetic retinopathy, our results suggest that loss of Tubedown expression may contribute to the development of retinopathy through disregulated retinal endothelial cell permeability.
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