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The role of lox and LOXL2 in inflammation and fibrosis in a laser induced mouse model
Author(s) -
VAN DE VEIRE S
Publication year - 2009
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2009.4232.x
Subject(s) - elastin , lysyl oxidase , fibrosis , sirius red , macular degeneration , cd31 , medicine , pathology , choroidal neovascularization , inflammation , retina , retinal , masson's trichrome stain , neovascularization , retinal degeneration , extracellular matrix , ophthalmology , immunohistochemistry , biology , angiogenesis , immunology , cancer research , microbiology and biotechnology , neuroscience
Abstract Purpose Lysyl oxidase (LOX) and lysyl oxidase‐like protein 2 (LOXL2) are involved in the cross‐linking of collagen and elastin in the extracellular space. The aim of this study was to investigate the expression LOX and LOXL2 in the eye (choroidea and retina) after laser‐induced chroidal neovascularization (CNV). We also want to check the anti‐angiogenic, anti‐inflammatory and anti‐fibrotic efficacy of anti‐LOX and anti‐LOXL2 antibody in a mouse model of age related macular degeneration (ARMD). Methods CNV will be induced in 8 to 10 weeks old C75Bl/6 mice, by placing 3 laser spots at 9, 12 and 3 o’clock position (50µm, 0.05 s and 400mW). Two daily injection with LOX(L) antibodies or control solution (PBS‐Tween 20%) will be given intraperitoneally from day 0 after lasering until day 34. Immediately after death, both eyes will be enucleated. One eye will be used to check RNA‐expression of LOX and LOXL. The other eye will be used to perform different immunohistochemical stainings (HE, Sirius Red, Trichrome, CD31, CD45 and LOX(L)). Results Preliminary results showed a significant increase of LOX and LOXL2 in the choroid and retina after lasering compared to control. Conclusion ARMD remains the most common cause of irreversible vision loss in people aged 50 years and older, due to (sub‐)retinal neovascularisation and scarring. It is already known that LOX and LOXL are playing a role in the cross linking of collagen and elastin, leading to an increase of fibrosis, and there is growing evidence that these molecules also play a role in neovascularisation. Therefore, a therapeutic potential of anti‐LOX and/or anti‐LOXL therapy can open new perspectives to treat CNV.