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E. Vandewalle, T. Van Bergen, S. Van de Veire, L. Moons, S. Fevery, V. Smith, S. Ogg, I. Stalmans; Role of Lox(l) in the Eye After Laser Photocoagulation in a Mouse Model for Age Related Macular Degeneration. Invest. Ophthalmol. Vis. Sci. 2009;50(13):771.
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Lysyl oxidase (LOX) and lysyl oxidase-like proteins (LOXL) are known to be involved in the cross-linking of collagen and elastin in the extracellular space. Therefore, these proteins play a major role in the process of fibrosis. This study was designed to elucidate the role of LOX and LOXL2 in inflammation and fibrosis after choroidal neovascularization (CNV).
CNV was induced by placing 3 laser spots at 9, 12 and 3 o’clock position (50µm, 0.05 s and 400mW) in 8 to 10 weeks old C75Bl/6 mice. Mice were sacrificed 4, 7, 14 and 28 days after laser. LOX and LOXL2 expression in choroid and retina was analyzed by using quantitative real time RT-PCR. Inflammation was studied by an immunohistochemical staining for CD45; fibrosis was evaluated by a Sirius Red and Trichrome staining.
Both LOX and LOXL2 were significantly increased in choroid and retina of lasered mice. LOX was 3.2, 1.75, 1.3 and 2 times upregulated on day 4, 7, 14 and 28 after laser compared to the relative expression of LOX in non-lasered eyes (P<0.05). LOXL2 was 1.6, 1.3, 1.1 and 1.5 times upregulated on day 4, 7, 14 and 28 after laser versus LOXL2 expression in non-lasered eyes (P<0.05) On day 4 after laser, the number of inflammatory cells was increased by 11% compared to the other time-points. Both Sirius Red and Thrichrome staining showed a significant increase of collagen deposition in the choroid on day 14 (34%) and 28 (38%) after laser compared to day 4 (7%) and 7 (14%) (P<0.05).
The upregulation of LOX and LOXL2 suggests that these molecules play a role in the process of inflammation and fibrosis after the induction of choroidal neovascularization. This finding can open new perspectives in the treatment of age-related macular degeneration by inhibiting LOX and LOXL.
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