April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Anti-Ras Molecule Inactivates Experimental Retinal Neovascularization After Intravitreal Non-Biodegradable VEGF/bFGF Implant in the Rabbit Model
Author Affiliations & Notes
  • Corinne G Wong
    Ophthalmic Drug Dev, SCLERA LLC, Carlsbad, CA
  • Kathryn Osann
    Ophthalmic Drug Dev, SCLERA LLC, Carlsbad, CA
    UC Irvine College of Medicine, Irvine, CA
  • Hung Tao Hsu
    Ophthalmic Drug Dev, SCLERA LLC, Carlsbad, CA
  • Footnotes
    Commercial Relationships Corinne Wong, None; Kathryn Osann, None; Hung Tao Hsu, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1965. doi:
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      Corinne G Wong, Kathryn Osann, Hung Tao Hsu; Anti-Ras Molecule Inactivates Experimental Retinal Neovascularization After Intravitreal Non-Biodegradable VEGF/bFGF Implant in the Rabbit Model. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1965.

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

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Abstract
 
Purpose
 

Previous studies demonstrate the unique induction of progressive experimental florid retinal neovascularization from intravitreal sustained simultaneous release of both VEGF & bFGF from a non-biodegradable implant in pigmented rabbit. The goal of this study is to assess the utility of an anti-RAS compound in decreasing experimental retinal NV after intravitreal administration.

 
Methods
 

Dutch belt rabbits (N = 12) weighing between 2 and 3 kg were utilized. One group (N = 6) was implanted intravitreally with blanks while the other group (N = 6) was given the VEGF/bFGF implants. Color fundus photography and fluorescein angiography (FA) were performed at weeks 1,2,3, and 4. Analysis of leakage was based on a scale of 0 to 4 on a weekly basis. Enucleation at week 4 was done with general histologic evaluation being performed on hematoxylin and eosin-stained retinal sections.

 
Results
 

Experimental florid retinal NV is inactivated by an anti-RAS compound that was injected once intravitreally after the VEGF/bFGF implants were inserted. Photos demonstrate after four weeks how retinal NV is prevented after intravitreal anti-RAS administration in comparison to animals with florid retinal NV not given the anti-RAS compound.

 
Conclusions
 

These results demonstrate the utility of anti-RAS compounds for preventing retinal NV in the rabbit model. Further studies will determine the ability of such compounds to ameliorate proliferative diabetic retinopathy. Finally such studies also will define how anti-RAS compounds can be utilized against choroidal NV for wet AMD. Wong CG, Rich KA, Liaw LHL, Hsu HT, and Berns MW. Intravitreal VEGF and bFGF produce florid retinal neovasculariation and hemorrhage in the rabbit. Curr Eye Res 22:150-157 (2001). Erb-Ho M, Sioulis CE, Kuppermann BD, Osann K, and Wong CG. Differential retinal angiogenic response to sustained intravitreal release of VEGF & bFGF in different pigmented rabbit breeds. Curr Eye Res 24: 245-252 (2002).

  
Keywords: 700 retinal neovascularization • 499 diabetic retinopathy • 453 choroid: neovascularization  
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