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N.Z. Gregori, S.W. Cousins, E.P. Hernandez, A. Caicedo, D.G. Espinosa–Heidmann; Upregulation of hypoxia induced genes in experimental branch retinal vein occlusion . Invest. Ophthalmol. Vis. Sci. 2004;45(13):5227. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Both retinal artery occlusion and retinal vein occlusion can be associated with retinal ischemia and hypoxia. However, artery occlusion is usually associated with retinal atrophy as vein occlusion is associated with vascular leakage and neovascularization. We sought to compare differences in upregulation of hypoxia–induced genes in experimental models of branch retinal artery occlusion and branch retinal vein occlusion. Methods: C57BL/6 mice (tyrosinase negative albinos) received intravenous injection of Rose Bengal followed by Argon laser photocoagulation of all branch arteries, all branch veins or sham laser treatment. Twenty–four hours later, the retinas were removed and messenger RNA extracted. RT–PCR was performed to analyze five hypoxia–induced genes including GLUT–1, NOS–2, Flt–1, MMP–9, and heme–oxygenase. Results:As expected, retinas with experimental branch artery occlusion demonstrated marked upregulation of heme–oxygenase (20.3 fold compared to normal) NOS–2 (23.6 fold), MMP–9 (2.6 fold increase) and GLUT–1 (2.0 fold increase). Surprisingly, branch retinal vein occlusion demonstrated similar magnitude upregulation in hypoxia–induced genes, including heme–oxygenase (17.3 fold increase), NOS–2 (6.8 fold increase), MMP–9 (1.5 fold increase) and GLUT–1 (2.3 fold increase). Neither model demonstrated significant increase in VEGF receptor (Flt–1). Conclusions: Experimental artery occlusion and experimental vein occlusion demonstrate similar magnitude of induction of hypoxia–induced gene expression. Comparisons of difference between gene expression and other factors may lead to better understanding of the pathogenesis of different complications in these two vascular disorders.
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