April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Exacerbated Choroidal Neovascularization In Nidogen-1 Deficient Mice
Author Affiliations & Notes
  • Irina Semkova
    Ophthalmology, Charite, University Medicine Berlin, Berlin, Germany
  • Dimitrios Karagiannis
    Ophthalmology, Charite, University Medicine Berlin, Berlin, Germany
  • Norbert Kociok
    Ophthalmology, Charite, University Medicine Berlin, Berlin, Germany
  • Antonia M. Joussen
    Ophthalmology, Charite, University Medicine Berlin, Berlin, Germany
  • Footnotes
    Commercial Relationships  Irina Semkova, None; Dimitrios Karagiannis, None; Norbert Kociok, None; Antonia M. Joussen, None
  • Footnotes
    Support  Funding DFG Jo 324 / 4-1, Jo 324 / 6-1 and 6-2, Jo 324-10-1, DFG SPP 1088-4, DFG SFB 612, BMFZ University of Düsseldorf, Stiftung für Altersforschung University of Düsseldorf
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 1781. doi:
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    • Get Citation

      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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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 
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