April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Intravitreal Bevacizumab in a Mouse Model of Laser Induced CNV
Author Affiliations & Notes
  • B. Meyer-Ruesenberg
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • A. Wiermann
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • S. Bigdon
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • M. Thill
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • R. Grierson
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • G. Richard
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • O. Zeitz
    Department of Ophthalmology, Universitaetsklinikum Hamburg-Eppendorf, Hamburg, Germany
  • Footnotes
    Commercial Relationships  B. Meyer-Ruesenberg, None; A. Wiermann, None; S. Bigdon, None; M. Thill, None; R. Grierson, None; G. Richard, None; O. Zeitz, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 74. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      B. Meyer-Ruesenberg, A. Wiermann, S. Bigdon, M. Thill, R. Grierson, G. Richard, O. Zeitz; Intravitreal Bevacizumab in a Mouse Model of Laser Induced CNV. Invest. Ophthalmol. Vis. Sci. 2009;50(13):74.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : Robust animal models for CNV and anti-VEGF therapy are required to gain a more detailed insight into the mechanisms of CNV. It was shown that Bevacizumab (Avastin®) inhibits corneal angiogenesis in a mouse model (Bock F et al., IOVS 2007) although the interaction between Bevacizumab and murine VEGF seems to be very weak (Yu L et al., IOVS 2008). This study was undertaken to evaluate the effect of intravitreal Bevacizumab on the dimensions of laser induced choroidal neovascularisation (CNV) in a mouse model.

Methods: : Adult C57BL/6J mice underwent argon laser photocoagulation in one eye to induce choroidal neovascularisation. They received four separate laser spots per eye around the optic nerve head. 16 mice were divided into two groups (treatment or control). Immediately after laser coagulation 1 µl of Bevacizumab (25 mg/ml, treatment group) or balanced salt solution (BSS, control group) was injected into the vitreous cavity. 14 days later the mice were sacrificed and their eyes explanted. After fixation overnight in 4% paraformaldehyde they were transferred into phosphate buffered saline (PBS). The eyes were freed from surrounding tissues and choroid flatmounts were prepared. Lectin from Bandeiraea simplicifolia was used for fluorescent labelling of the CNVs. They were visualized by fluorescence microscopy and the size of each CNV was measured using an image analyzing software (Image Tool®). For statistic calculation, CNVs were averaged for each eye. Results (dimensionless) were analyzed for statistic significance using a multivariate ANOVA (SPSS®).

Results: : The injection of Bevacizumab did not lead to a reduction of the size of the CNVs (486077 ± 101317 (control) versus 649847 ± 284181 (treatment group)). There was no significant difference shown between the size of the CNVs in both groups (p=0,185).

Conclusions: : The humanized VEGF antibody Bevacizumab is not capable of inhibiting the development of laser induced CNV in mice. To achieve the goal of a rodent animal model for anti-VEGF therapy, the use of specific murine anti-VEGF antibodies may be an option.

Keywords: retina 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×