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Differential gene expression in Ndph-knockout mice in retinal development.

Nikolaus F Schäfer1, Ulrich F O Luhmann, Silke Feil

  • 1Division of Medical Molecular Genetics and Gene Diagnostics, Institute of Medical Genetics, University of Zurich, Schwerzenbach, Switzerland.

Investigative Ophthalmology & Visual Science
|November 4, 2008
PubMed
Summary

Norrin deficiency in mice causes changes in retinal gene expression, including increased plasmalemma vesicle associated protein (Plvap), which may contribute to exudative vitreoretinopathies and blindness.

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Area of Science:

  • Ophthalmology
  • Genetics
  • Developmental Biology

Background:

  • Mutations in the NDP gene cause exudative vitreoretinopathies, a group of blinding conditions.
  • Norrin (NDP protein) is crucial for proper eye development and vascularization.

Purpose of the Study:

  • Investigate differential gene expression in the absence of Norrin in developing mouse retinas.
  • Elucidate early pathogenic events in Norrin-deficient eyes.

Main Methods:

  • Comparative gene expression analysis using microarrays on postnatal day 7 retinas from Norrin knockout mice.
  • Quantitative real-time PCR for verification.
  • Immunohistochemistry for plasmalemma vesicle associated protein (Plvap).

Main Results:

  • Decreased gene transcription of Slc38a5, ApoD, and Agtrl1 in Norrin knockout retinas.
  • Increased transcript levels of Adm and Plvap compared to wild-type.
  • Ectopic Plvap expression observed in the retinal vasculature of knockout mice.

Conclusions:

  • Norrin plays a role in retinal vascular development.
  • Altered expression of Plvap and Slc38a5 in Norrin knockout mice contributes to disease pathogenesis.
  • Ectopic Plvap expression correlates with disease symptoms in mice and humans.