Abstract
Purpose: :
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.
Methods: :
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.
Results: :
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.
Conclusions: :
The lack of nidogen-1 leads to disruption of RPE/BrM integrity and exacerbated CNV formation after laser treatment.
Keywords: age-related macular degeneration • Bruch's membrane • retinal pigment epithelium