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Irina Semkova, Dimitrios Karagiannis, Norbert Kociok, Antonia M. Joussen; Exacerbated Choroidal Neovascularization In Nidogen-1 Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2011;52(14):1781.
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Changes in the composition and integrity of Bruch’s membrane (BrM) in the aged eye may be the reason for the pigment epithelium detachment and formation of subretinal fibrovascular deposits.
Using a laser injury model, we induced choroidal neovascularisation (CNV) in mice lacking nidogen-1, nidogen-2 and the respective wild type (WT) controls. Distribution and expression of nidogen binding basal membrane proteins including laminin-γ1, collagen-IV, and perlecan were investigated by immunochemistry in the absence of nidogen-1 and -2. CNV lesions were analyzed in vivo by fluorescein angiography and histological on flat mounts and paraffin sections.
Areas of separation of RPE cells from the BrM, increased thickness and breaks of the BrM were observed in nidogen-1-/- and particularly in nidogen-2-/- mice. After laser photocoagulation, fluorescein angiography and histology on paraffin sections showed exacerbated CNV lesions in nidogen-1 deficient compared to the nidogen-2 and WT mice.
The lack of nidogen-1 leads to disruption of RPE/BrM integrity and exacerbated CNV formation after laser treatment.
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