rss
Br J Ophthalmol 2000;84:1415-1419 doi:10.1136/bjo.84.12.1415
  • Original Article
    • Laboratory science

The APO*E3-Leiden mouse as an animal model for basal laminar deposit

  1. Mike Kliffena,
  2. Esther Lutgensd,
  3. Mat J A P Daemene,
  4. Ebo D de Muinckd,
  5. Cornelia M Mooya,b,
  6. Paulus T V M de Jongc,f
  1. aDepartment of Pathology, Erasmus University, Rotterdam, Netherlands, bDepartment of Ophthalmology, cDepartment of Epidemiology and Biostatistics, dDepartment of Cardiology, University of Maastricht, Netherlands, eDepartment of Pathology, fNetherlands Ophthalmic Research Institute and Department of Ophthalmology Academic Medical Center, Amsterdam, Netherlands
  1. Dr M Kliffen, Department of Pathology, JNI room 206, Erasmus University, PO Box 1738, 3000 DR Rotterdam, Netherlandskliffen{at}path.fgg.eur.nl
  • Accepted 10 July 2000

Abstract

AIM To investigate the APO*E3-Leiden mouse as an animal model for age related maculopathy (ARM) related extracellular deposits.

METHODS Eyes were obtained from APO*E3-Leiden transgenic mice on a high fat/cholesterol (HFC) diet (n=12) or on a normal mouse chow (n=6), for 9 months. As controls, eyes were collected from APO-E knockout mice on the same diets. From each mouse one eye was processed for microscopic evaluation and immunohistochemistry with a polyclonal antibody directed against human apo-E. Electron microscopy was also performed.

RESULTS All 12 eyes of the APO*E3-Leiden mice on an HFC diet contained basal laminar deposit (BLD; class 1 to class 3), whereas two of six APO*E3-Leiden mice on normal chow showed BLD class 1. The ultrastructural aspects of this BLD were comparable with those seen in early BLD in humans, and BLD showed immunoreaction with anti-human-apo-E antibodies. No BLD was found in any of the control mice. Drusen were not detected in any of the mice.

CONCLUSION These results indicate that APO*E3-Leiden mice can be used as animal model for the pathogenesis of BLD, and that a HFC diet enhances the accumulation of this deposit. Furthermore, this study supports the previously suggested involvement of dysfunctional apo-E in the accumulation of extracellular deposits in ARM.

Footnotes

    This Article

    1. Abstract
    2. Full text
    3. PDF

    Responses

    1. Submit a response
    2. No responses published

    Register for free content

    The full back archive is now available for all BMJ Journals. Institutional subscribers may access the entire archive as part of their subscription. Personal subscribers will also have access to all content when logged in. Non-subscribers who register have free access to all articles published before 2006 right back to volume 1 issue 1. Register here to access the free archive of all BMJ Journals.

    Don't forget to sign up for content alerts so you keep up to date with all the articles as they are published.