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S. Wang, Z. Wu, J.G. Brantley, G.B. Vanden Heuvel, N. Sheibani; The Cux-1 Transgenic Mice Display Reduced Retinal Vascular Density and Undergo Retinal Degeneration . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2036.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Deregulated expression of the homeobox gene Cux-1 in transgenic mice results in multiorgan hyperplasia through down-regulation of the cyclin kinase inhibitor, p27Kip1, expression. This report investigates the role of Cux-1 expression on retinal development and vascularization. Methods: Retinal morphology was examined by preparation of histological sections from three-weeks and six-weeks old mice. Retinal vessels and vascular density were assessed utilizing retinal trypsin digests. The vascular endothelial cell, pericytes, and astrocytes were detected by staining wholemount retinas with antibodies to PECAM-1, NG-2, and glial fibrillary acidic protein (GFAP), respectively. Results: Histological examination showed total loss of photoreceptors throughout the retina in Cux-1 transgenic mice by six-weeks of age. The retinal trypsin digests demonstrated a lower retinal vascular density and thinner arterioles in Cux-1 transgenic mice compared to the wild type mice. GFAP staining of retina wholemounts revealed increased number of astrocytes in Cux-1 transgenic mice. Conclusion: We demonstrate that Cux-1 is an important regulator of retinal development and vascularization and its aberrant expression results in vascular abnormalities and retinal degeneration.
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