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Y. Inomata, A. Hirata, E. Takahashi, M. Honjo, H. Sato, T. Sawamura, M. Takeya, H. Tanihara; Lectin–Like Oxidized Low–Density Lipoprotein Receptor–1 (LOX–1) Contributes to the Formation of Choroidal Neovascularization . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5296.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose:To determine if lectin–like oxidized low–density lipoprotein receptor–1 (LOX–1) contributes to the formation of experimental choroidal neovascularization (CNV). Methods:CNV was induced in wild–type and LOX–1–deficient mice by krypton laser photocoagulation. The time–course of LOX–1 expression after laser treatment was determined by real time RT–PCR. Two weeks after laser treatment, the extent of CNV was evaluated on fluorescein angiography (FA), hematoxylin–eosin stained serial sections, and flat–mount analysis of CNV surface area using FITC–lectin. Results:Expression of LOX–1 mRNA was detected in the CNV lesions at 6 hr after laser treatment and peaked at 48 hr, after which it slowly declined. Two weeks after laser treatment, 14 of 24 burns (58%) in LOX–1–deficient mice showed fluorescein leakage in wild type mice compared with 27 of 29 burns (93%) in wild type mice in FA examination. In serial sections analysis, the CNV lesions of LOX–1–deficient mice showed that relative thickness was reduced compared with wild–type mice (P = 0.02). In flat–mount analysis of CNV, the size of CNV was significantly reduced in LOX–1–deficient mice than wild–type mice (P < 0.005). Conclusions: The present study demonstrated that the expression of LOX–1 mRNA is up–regulated after laser treatments for the creation of experimental CNV in mice. A series of experiments revealed that there are significant differences in the formation of CNV and vascular leakage between wild–type and LOX–1–deficient mice. It has been suggested that LOX–1 is involved in the CNV formation.
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