May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Anti-PlGF (Placental Growth Factor) Reduces Choroidal Neovascularization in a Mouse Model of Age-Related Macular Degeneration (ARMD)
Author Affiliations & Notes
  • S. Van de Veire
    KULeuven, Leuven, Belgium
    Ophthalmology,
  • S. Vinores
    Ophthalmology, John Hopkins, Baltimore, Maryland
  • A. Peric
    KULeuven, Leuven, Belgium
    Center for Transgene Technology & Gene Therapy,
  • M. Mazzone
    KULeuven, Leuven, Belgium
    Center for Transgene Technology & Gene Therapy,
  • G. Moons
    KULeuven, Leuven, Belgium
    Biology,
  • J.-M. Stassen
    KULeuven, Leuven, Belgium
    Center for Transgene Technology & Gene Therapy,
  • A. Noel
    Ophthalmology, University of Liege, Liege, Belgium
  • I. Stalmans
    KULeuven, Leuven, Belgium
    Ophthalmology,
  • P. Carmeliet
    KULeuven, Leuven, Belgium
    Center for Transgene Technology & Gene Therapy,
  • Footnotes
    Commercial Relationships  S. Van de Veire, None; S. Vinores, None; A. Peric, None; M. Mazzone, None; G. Moons, None; J. Stassen, Thrombogenics, I; A. Noel, None; I. Stalmans, None; P. Carmeliet, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5411. doi:https://doi.org/
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      S. Van de Veire, S. Vinores, A. Peric, M. Mazzone, G. Moons, J.-M. Stassen, A. Noel, I. Stalmans, P. Carmeliet; Anti-PlGF (Placental Growth Factor) Reduces Choroidal Neovascularization in a Mouse Model of Age-Related Macular Degeneration (ARMD). Invest. Ophthalmol. Vis. Sci. 2008;49(13):5411. doi: https://doi.org/.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Purpose: : To evaluate whether and through which mechanism PlGF blockage can inhibit choroidal neovascularization (CNV)in a mouse model of ARMD.

Methods: : CNV was induced in mice by placing 3 Argon laser burns on the choroid. In a first experiment we compared CNV formation between PlGF knock-out and wild type mice. Secondly, wild-type mice were injected intraperitoneally with 6, 12, 25 or 50 mg/kg of either an anti-PlGF-antibody, an anti-VEGF receptor-2 (VEGFR2) antibody, a combination of both or an irrelevant control antibody. The CNV lesions were evaluated on flat mounts and histological cross-sections. The amount of endothelial cells and inflammatory cells in the lesions was morphometrically analyzed after immunostaining for CD31 or F4/80 respectively. Thirdly, combination therapy with anti-PlGF and anti-VEGF receptor-2 was given to seek for additional inhibition of neovascularization.

Results: : CNV formation was significantly reduced in PlGF knockout mice. Anti-PlGF significantly inhibited choroidal neovascularization, comparably to anti-VEGFR2 (p<0.05). Moreover, a combination treatment of anti-PlGF and anti-VEGFR2 further suppressed CNV (p<0.05). Finally, a significant reduction in the number of inflammatory cells was observed in the lesions treated with anti-PlGF (p<0.05), but not in anti-VEGFR2 treated mice.

Keywords: age-related macular degeneration • choroid: neovascularization • growth factors/growth factor receptors 
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